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Universidad de Cantabria
1.
Francés Romero, Raquel.
Neuropathic pain induced by sciatic nerve injury involves epigenetic changes and chromatolytic damage in the somatosensory nervous system. Effects of miR-30c-5p gain and loss of function.
Degree: 2019, Universidad de Cantabria
URL: http://hdl.handle.net/10902/16191 
► ABSTRACT: Neuropathic pain (NP) is a debilitating chronic syndrome that is often refractory to currently available analgesics. The maintenance of NP encompasses long term pathological…
(more)
▼ ABSTRACT:
Neuropathic pain (NP) is a debilitating chronic syndrome that is often refractory to currently available analgesics. The maintenance of NP encompasses long term pathological plasticity in the nervous system that may be explained by alterations in the epigenetic mechanisms and cellular processes that underlie this disease. In this thesis, we investigated the involvement of epigenetic mechanisms in
neuropathic pain establishment and chronification and the effects of modulating miR-30c-5p in the somatosensory nervous system. The transcript levels of DNA methyltransferase-3A and 3B were significantly up-regulated in the spinal dorsal horn and dorsal root ganglia from
neuropathic rats. This upregulation was potentiated when
neuropathic rats were treated with a miR-30c-5p inhibitor. In parallel, both structures exhibited increased methylation at cytosine in CpG islands. By luciferase assay, we demonstrated a post-transcriptional regulation for DNMT3B and DNMT3A by miR-30c-5p.
Furthermore, we demonstrated that NP induces an increase in the chromatolytic damage suffered by DRG neurons. This phenomenon was potentiated when
neuropathic rats were treated with a miR-30c-5p mimic. We showed that miR-30c-5p treatment induces reorganization and loss of nucleolar transcription units, segregation of dense fibrillar and granular components and a depletion of cajal bodies. We propose that miR-30c-5p modulation in NP plays an essential role in the epigenetic mechanism and cellular processes that underlie this disease.
Advisors/Committee Members: Hurlé González, María Amor (advisor), Universidad de Cantabria (other).
Subjects/Keywords: Neuropathic pain
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APA (6th Edition):
Francés Romero, R. (2019). Neuropathic pain induced by sciatic nerve injury involves epigenetic changes and chromatolytic damage in the somatosensory nervous system. Effects of miR-30c-5p gain and loss of function. (Doctoral Dissertation). Universidad de Cantabria. Retrieved from http://hdl.handle.net/10902/16191
Chicago Manual of Style (16th Edition):
Francés Romero, Raquel. “Neuropathic pain induced by sciatic nerve injury involves epigenetic changes and chromatolytic damage in the somatosensory nervous system. Effects of miR-30c-5p gain and loss of function.” 2019. Doctoral Dissertation, Universidad de Cantabria. Accessed January 28, 2021.
http://hdl.handle.net/10902/16191.
MLA Handbook (7th Edition):
Francés Romero, Raquel. “Neuropathic pain induced by sciatic nerve injury involves epigenetic changes and chromatolytic damage in the somatosensory nervous system. Effects of miR-30c-5p gain and loss of function.” 2019. Web. 28 Jan 2021.
Vancouver:
Francés Romero R. Neuropathic pain induced by sciatic nerve injury involves epigenetic changes and chromatolytic damage in the somatosensory nervous system. Effects of miR-30c-5p gain and loss of function. [Internet] [Doctoral dissertation]. Universidad de Cantabria; 2019. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/10902/16191.
Council of Science Editors:
Francés Romero R. Neuropathic pain induced by sciatic nerve injury involves epigenetic changes and chromatolytic damage in the somatosensory nervous system. Effects of miR-30c-5p gain and loss of function. [Doctoral Dissertation]. Universidad de Cantabria; 2019. Available from: http://hdl.handle.net/10902/16191
University of Alberta
2.
Kim, Helena J.
Effects of long-term inhibition of EAAT2 on the excitability
of spinal dorsal horn neurons.
Degree: MS, Centre for Neuroscience, 2010, University of Alberta
URL: https://era.library.ualberta.ca/files/bv73c055p
► This thesis examined the effects of long-term inhibition of excitatory amino acid transporter 2 (EAAT2) on the excitability of dorsal horn neurons in defined-medium organotypic…
(more)
▼ This thesis examined the effects of long-term
inhibition of excitatory amino acid transporter 2 (EAAT2) on the
excitability of dorsal horn neurons in defined-medium organotypic
slice cultures (DMOTCs). Previous reports suggest that inhibition
of EAAT2 may be involved in development of neuropathic pain induced
by brain-derived neurotrophic factor (BDNF). Experiments were
carried out using confocal Ca2+ imaging to assess the excitability
of dorsal horn neurons. Long-term treatment with EAAT2 blocker,
dihydrokainate (DHK), prominently increased the neuronal
excitability. Long-term exposure to DHK had a significant effect on
NMDA, AMPA and metabotropic glutamate subtype 1 (mGluR1) receptors.
Lastly, long-term treatment with BDNF and DHK increased activity of
AMPA receptors but only DHK significantly increased activity of
NMDA receptors. These findings suggest inhibition of EAAT2 and BDNF
may have different pathways to promote neuropathic pain and
modulating the activity of EAAT2 may be a novel therapeutic
approach for neuropathic pain.
Subjects/Keywords: Neuropathic pain; EAAT2
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APA (6th Edition):
Kim, H. J. (2010). Effects of long-term inhibition of EAAT2 on the excitability
of spinal dorsal horn neurons. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/bv73c055p
Chicago Manual of Style (16th Edition):
Kim, Helena J. “Effects of long-term inhibition of EAAT2 on the excitability
of spinal dorsal horn neurons.” 2010. Masters Thesis, University of Alberta. Accessed January 28, 2021.
https://era.library.ualberta.ca/files/bv73c055p.
MLA Handbook (7th Edition):
Kim, Helena J. “Effects of long-term inhibition of EAAT2 on the excitability
of spinal dorsal horn neurons.” 2010. Web. 28 Jan 2021.
Vancouver:
Kim HJ. Effects of long-term inhibition of EAAT2 on the excitability
of spinal dorsal horn neurons. [Internet] [Masters thesis]. University of Alberta; 2010. [cited 2021 Jan 28].
Available from: https://era.library.ualberta.ca/files/bv73c055p.
Council of Science Editors:
Kim HJ. Effects of long-term inhibition of EAAT2 on the excitability
of spinal dorsal horn neurons. [Masters Thesis]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/bv73c055p
University of Sydney
3.
Tam, Denise June.
Role of Glycinergic Neurotransmission in Neuropathic Pain
.
Degree: 2016, University of Sydney
URL: http://hdl.handle.net/2123/16314
► The Gate Control Theory of Pain highlights an interconnected network of myelinated and unmyelinated fibres within the dorsal horn (Melzack & Wall, 1965). Currently there…
(more)
▼ The Gate Control Theory of Pain highlights an interconnected network of myelinated and unmyelinated fibres within the dorsal horn (Melzack & Wall, 1965). Currently there are a number of proposed theories to explain the mechanism by which pain is developed, one of which is the theory of disinhibition whereby a reduction of inhibitory neurotransmission leads to over-excitation within the central nervous system (Guo & Hu, 2014; Zeilhofer, 2005). Evidence within my supervisor’s laboratory has identified glycinergic inhibitory neurotransmission to be a key component in the development of neuropathic pain. This study aimed to identify the main reasons for these reductions in inhibitory neurotransmission shown within lamina II of the dorsal horn. It is hypothesised that inhibitory neurotransmission is lost following injury leading to over-excitation within the dorsal horn. The experiments performed within this study were optimised through following vigorous testing procedures often requiring multiple trial and error attempts prior to the development of both valid and reliable results. PKCγ immunoreactive neurons are found within lamina II of the dorsal horn are classified into distinct morphological categories, and are involved in the filtering of nociceptive and mechanical input (Martin, Liu, Wang, Malmberg & Basbaum, 1999). This study showed distinct changes of PKCγ immunoreactive neurons following a neuropathic pain injury suggestive of the possibility of changes to the neural circuitry within the dorsal horn. Furthermore GAD67 neurons in lamina II of the dorsal horn was analysed to identify whether this can be used as a method of identifying changes in presynaptic neurons following neuropathic injury but failed to yield significant results. In conclusion immunohistological studies are found to be limited in providing physiological information on neurons within the dorsal horn. As a result future experimentations seeking alternative techniques must be sought to confirm the significance the results in the study.
Subjects/Keywords: glycine;
neuropathic pain
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APA (6th Edition):
Tam, D. J. (2016). Role of Glycinergic Neurotransmission in Neuropathic Pain
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/16314
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Tam, Denise June. “Role of Glycinergic Neurotransmission in Neuropathic Pain
.” 2016. Thesis, University of Sydney. Accessed January 28, 2021.
http://hdl.handle.net/2123/16314.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tam, Denise June. “Role of Glycinergic Neurotransmission in Neuropathic Pain
.” 2016. Web. 28 Jan 2021.
Vancouver:
Tam DJ. Role of Glycinergic Neurotransmission in Neuropathic Pain
. [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2123/16314.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tam DJ. Role of Glycinergic Neurotransmission in Neuropathic Pain
. [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/16314
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
4.
Fiore, Nathan Troy.
Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states
.
Degree: 2019, University of Sydney
URL: http://hdl.handle.net/2123/20984
► Nerve damage leads to the development of disabling neuropathic pain in susceptible individuals, where patients present with pain as well as co-morbid behavioural changes, such…
(more)
▼ Nerve damage leads to the development of disabling neuropathic pain in susceptible individuals, where patients present with pain as well as co-morbid behavioural changes, such as anhedonia, decreased motivation and depression. The pathophysiology of neuropathic pain remains unknown, however accumulating evidence suggests that neuroimmune interactions play a key role in its pathogenesis and development of co-morbid behavioural disturbances. Complex regional pain syndrome (CRPS) is a debilitating neuropathic disorder where trauma to a limb results in chronic pain. Mass cytometry (CyTOF) was used to systematically analyse circulating immune cells with a panel of 38 phenotypic and activation markers in the blood of CRPS patients and healthy controls. CyTOF revealed an expansion and increased activation of signalling pathways in several distinct populations of central memory CD8+ and CD4+ T lymphocytes. Regarding emotional state, CD8+ T lymphocytes were correlated with clinical scores for stress and CD4+ Th1 lymphocytes correlated with clinical scores for anxiety. There was also a reduction in circulating Dendritic cells (DC), indicative of DC tissue trafficking and potential involvement in lymphocyte activation. These data highlight a pathogenic role for T lymphocyte mediated chronic inflammation in CRPS and co-morbid behavioural disabilities. To further explore to role of neuroimmune interactions in the development of neuropathic pain and co-morbid behavioural changes, a rodent nerve injury model was utilized to evaluate whether individual differences in radial maze behaviour and neuroimmune interactions in the hippocampus (HP) and medial prefrontal cortex (mPFC) occurred in rats after sciatic nerve chronic constriction injury (CCI). CCI reduced mechanical withdrawal thresholds in all rats, whilst pellet-seeking behaviours were altered in some but not all rats. One group, termed ‘No effect’, had no behavioural changes compared to sham rats. Another group, termed ‘Acute effect’, had a temporary alteration to their exploration pattern, displaying more risk-assessment behaviour in the early phase post-injury. In a third group, termed ‘Lasting effect’, exploratory behaviours were remarkably different for the entire post-injury period, showing a withdrawal from pellet-seeking. Immunohistochemical analysis throughout the dorso-ventral axis of the HP revealed that the withdrawal from pellet-seeking observed in Lasting effect rats was concomitant with distinct glial-cytokine-neuronal adaptations within the contralateral ventral HP, including; increased expression of IL-1b and MCP-1; astrocyte atrophy and decreased area in the dentate gyrus (DG); reactive microglia and increased FosB/DFosB expression in the cornu ammonis (CA) subfield. These data highlight that glial-cytokine-neuronal adaptations in the ventral HP may mediate individual differences in radial maze behaviour following CCI. A follow up experiment explored whether pre-injury learning on the maze altered the effects of nerve injury on exploratory behaviour and…
Subjects/Keywords: Neuropathic pain;
Neuroinflammation
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Manager
APA (6th Edition):
Fiore, N. T. (2019). Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20984
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Fiore, Nathan Troy. “Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states
.” 2019. Thesis, University of Sydney. Accessed January 28, 2021.
http://hdl.handle.net/2123/20984.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Fiore, Nathan Troy. “Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states
.” 2019. Web. 28 Jan 2021.
Vancouver:
Fiore NT. Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states
. [Internet] [Thesis]. University of Sydney; 2019. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2123/20984.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Fiore NT. Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states
. [Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/20984
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
5.
Froimovitch, Daniel.
Genetic and Phenomic Determinants of Basal Mechano-sensitivity and Spread of Neuropathic Pain Following Transection of the Infraorbital Nerve in Mice.
Degree: 2011, University of Toronto
URL: http://hdl.handle.net/1807/30598
► Craniofacial nerve injury occasionally causes spread of mechanical hypersensitivity in humans. We modeled this abnormality by transecting the infraorbital nerve (IONX) in male and female…
(more)
▼ Craniofacial nerve injury occasionally causes spread of mechanical hypersensitivity in humans. We modeled this abnormality by transecting the infraorbital nerve (IONX) in male and female mice of the 23 AXB-BXA recombinant inbred lines and their progenitor strains, comparing their responsivity to 7 applications of a 0.2 gram Von Frey filament to the ears, paws and tail. When normalizing their mechano-responsivity on postoperative days 14 and 21 by the preoperative values, subtracting data of sham-operated from IONX mice, highly contrasting line/strain-specific differences were demonstrated. Similar line/strain-specific variability in the spread of mechano-allodynia to the paws post-IONX was demonstrated in our novel 3 minute place-avoidance paradigm, assessing parameters of mobility on a smooth surface versus a pro-allodynic granular surface. These genetically-controlled, widespread changes in mechano-sensitivity caused by IONX were minimally sexually dimorphic and mapped to intervals on chromosomes 5, 9, and 13. Further analysis is needed to identify the causative genes.
MAST
Advisors/Committee Members: Seltzer, Ze'ev, Physiology.
Subjects/Keywords: Neuropathic Pain; Pain Spread; Pain Genetics; 0719
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APA (6th Edition):
Froimovitch, D. (2011). Genetic and Phenomic Determinants of Basal Mechano-sensitivity and Spread of Neuropathic Pain Following Transection of the Infraorbital Nerve in Mice. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/30598
Chicago Manual of Style (16th Edition):
Froimovitch, Daniel. “Genetic and Phenomic Determinants of Basal Mechano-sensitivity and Spread of Neuropathic Pain Following Transection of the Infraorbital Nerve in Mice.” 2011. Masters Thesis, University of Toronto. Accessed January 28, 2021.
http://hdl.handle.net/1807/30598.
MLA Handbook (7th Edition):
Froimovitch, Daniel. “Genetic and Phenomic Determinants of Basal Mechano-sensitivity and Spread of Neuropathic Pain Following Transection of the Infraorbital Nerve in Mice.” 2011. Web. 28 Jan 2021.
Vancouver:
Froimovitch D. Genetic and Phenomic Determinants of Basal Mechano-sensitivity and Spread of Neuropathic Pain Following Transection of the Infraorbital Nerve in Mice. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1807/30598.
Council of Science Editors:
Froimovitch D. Genetic and Phenomic Determinants of Basal Mechano-sensitivity and Spread of Neuropathic Pain Following Transection of the Infraorbital Nerve in Mice. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/30598
University of Toronto
6.
Marciniak, Robert.
Design of an Approach to Characterize CD11b Cre x LoxP BDNF Deletion in Mice: Implications for Neuropathic Pain.
Degree: 2012, University of Toronto
URL: http://hdl.handle.net/1807/33440
► Background: An approach designed to characterize BDNF gene deletion within microglia of the dorsal horn of the spinal cord does not currently exist. Therefore, my…
(more)
▼ Background: An approach designed to characterize BDNF gene deletion within microglia of the dorsal horn of the spinal cord does not currently exist. Therefore, my goal was to develop methods to assess Cre- mediated BDNF deletion. To this end I designed and tested two different approaches focusing on the aspects of BDNF mRNA expression or genomic level gene deletion. Methods: Approach 1: BDNF messenger RNA was detected by in situ hybridization. Approach 2: BDNF gene deletion was detected by a positive signal semi-quantitative Polymerase Chain Reaction (PCR). Results: In situ hybridization detected spinal BDNF and regional changes in BDNF mRNA following PNI in wild-type mice. The BDNF PCR detected Cre-mediated BDNF deletions in transgenic animals. Conclusion: Two approaches have been developed and initial tests of these approaches show promising results and will provide valuable tools for researchers investigating BDNF deletion in transgenic animals.
MAST
Advisors/Committee Members: Salter, Michael, Dentistry.
Subjects/Keywords: BDNF; Neuropathic Pain; 0317
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APA (6th Edition):
Marciniak, R. (2012). Design of an Approach to Characterize CD11b Cre x LoxP BDNF Deletion in Mice: Implications for Neuropathic Pain. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/33440
Chicago Manual of Style (16th Edition):
Marciniak, Robert. “Design of an Approach to Characterize CD11b Cre x LoxP BDNF Deletion in Mice: Implications for Neuropathic Pain.” 2012. Masters Thesis, University of Toronto. Accessed January 28, 2021.
http://hdl.handle.net/1807/33440.
MLA Handbook (7th Edition):
Marciniak, Robert. “Design of an Approach to Characterize CD11b Cre x LoxP BDNF Deletion in Mice: Implications for Neuropathic Pain.” 2012. Web. 28 Jan 2021.
Vancouver:
Marciniak R. Design of an Approach to Characterize CD11b Cre x LoxP BDNF Deletion in Mice: Implications for Neuropathic Pain. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1807/33440.
Council of Science Editors:
Marciniak R. Design of an Approach to Characterize CD11b Cre x LoxP BDNF Deletion in Mice: Implications for Neuropathic Pain. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/33440
University of Toronto
7.
Elahipanah, Tina.
Identification of Candidate Genes for Neuropathic Pain at the Pain1 Locus on Mouse Chromosome 15.
Degree: 2010, University of Toronto
URL: http://hdl.handle.net/1807/25562
► Sciatic and saphenous neurectomy produces in mice a neuropathic pain-like behaviour (‘autotomy’). A/J mice express higher autotomy levels than C57BL6/J mice. A previous study used…
(more)
▼ Sciatic and saphenous neurectomy produces in mice a neuropathic pain-like behaviour (‘autotomy’). A/J mice express higher autotomy levels than C57BL6/J mice. A previous study used autotomy data for these strains and their 23 recombinant daughter inbred lines of the AXB-BXA set, to map a quantitative trait locus (QTL) for autotomy on chromosome 15. Since then, this QTL, named Pain1, was replicated twice. Since all three studies used a low-resolution genetic map based on microsatellites its confidence length precluded identification of candidate gene(s). To overcome this problem, I used a higher resolution SNP-based genetic map and refined Pain1’s peak location, identifying in it 80 candidate genes. But only Lynx1, Arc and Sharpin had sequence mismatches between A/J and C57BL6/J, known neural functions, and contrasting expression levels in DRGs and spinal cord of intact, sham-operated, and neurectomized mice of these lines. Meeting these criteria made them our best candidate genes for autotomy.
MAST
Advisors/Committee Members: Seltzer, Ze'ev, Physiology.
Subjects/Keywords: Neuropathic Pain; Gene; 0719
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APA (6th Edition):
Elahipanah, T. (2010). Identification of Candidate Genes for Neuropathic Pain at the Pain1 Locus on Mouse Chromosome 15. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/25562
Chicago Manual of Style (16th Edition):
Elahipanah, Tina. “Identification of Candidate Genes for Neuropathic Pain at the Pain1 Locus on Mouse Chromosome 15.” 2010. Masters Thesis, University of Toronto. Accessed January 28, 2021.
http://hdl.handle.net/1807/25562.
MLA Handbook (7th Edition):
Elahipanah, Tina. “Identification of Candidate Genes for Neuropathic Pain at the Pain1 Locus on Mouse Chromosome 15.” 2010. Web. 28 Jan 2021.
Vancouver:
Elahipanah T. Identification of Candidate Genes for Neuropathic Pain at the Pain1 Locus on Mouse Chromosome 15. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1807/25562.
Council of Science Editors:
Elahipanah T. Identification of Candidate Genes for Neuropathic Pain at the Pain1 Locus on Mouse Chromosome 15. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/25562
University of Adelaide
8.
Arman, Azim.
Advanced preclinical assessment of hyper-nociception.
Degree: 2020, University of Adelaide
URL: http://hdl.handle.net/2440/127165
► Neuropathic pain is a major health concern with a significant financial burden on the global society. This complex neuroimmune disorder has a significant reliance on…
(more)
▼ Neuropathic pain is a major health concern with a significant financial burden on the global society. This complex neuroimmune disorder has a significant reliance on cytokines, including IL-1β, in the pathogenesis of
neuropathic pain, due to neuroimmune reactions in spinal cord dorsal horn. Currently, there are methodological challenges for repeated Cerebrospinal fluid (CSF) sampling for cytokines in rodents including the terminality nature of CSF sampling which makes the in vivo longitudinal monitoring of the cytokine challenging. To address these challenges, this PhD thesis focuses on
neuropathic pain and a novel method applied to quantify the molecular mediators of the exaggerated nociception and specifically IL-1β in a preclinical model of mechanical allodynia. The introduction of this thesis contains two sections. Firstly,
neuropathic pain, the associated neuroimmune mediators and the relevance of cytokine signals is discussed. Of specific focus here is the role of Interleukin-1β (IL-1β) in exaggerated
pain states. The challenges of quantifying IL-1β in vivo and the importance this information will have for our understanding of the pathogenesis
neuropathic pain is presented. In the second section of the introduction, the need for new technology to enable these key biological measurements, with a focus on novel sensing interface-based techniques is reviewed. Of specific note are the functionalization processes applicable in immobilizing bio-receptors on a surgically (intrathecal)-compatible surface to capture a target molecule. The review will also cover the surgical approaches that will enable researchers to access the intrathecal space in rodents with the purpose of measuring intrathecal molecules. Together, these complementary tools, make the measurements of a hypothetical molecule, in this case IL-1β, possible in the spinal cord. In the third chapter, a method to quantify IL-1β in cerebrospinal fluid based on application of a stainless-steel based biosensor in live animals with high sensitivity is presented. These biosensors are functionalized using poly (ethylene glycol) methacrylate (PEGMA) as the tether molecules to immobilize capture antibody. In the fourth chapter, this method will be employed to have the longitudinal in vivo quantification of intrathecal IL-1β during a peripheral neuropathy, chronic constriction injury (CCI). In this chapter, the correlation between behavioural allodynia during the development and maintenance of nerve injury and the repeated sampling of intrathecal IL-1β over 14 days post injury is presented for the first time. In brief, CCI caused a significant increase in intrathecal IL-1β concentrations from day 0 to day 7 through day 14. In the fifth chapter, the literature on peripheral nerve injury models (sciatic based and spinal nerve based) will be systematically reviewed, and the main categories of biomarkers studied with this model of nerve injury will be presented. The results show that cytokines are the dominant biomarker analysed in the sciatic based neuropathies with…
Advisors/Committee Members: Hutchinson, Mark (advisor), Mustafa, Sanam (advisor), Schartner, Erik (advisor), Adelaide Medical School (school).
Subjects/Keywords: Neuropathic pain; cytokines; biomarkers
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APA (6th Edition):
Arman, A. (2020). Advanced preclinical assessment of hyper-nociception. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/127165
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Arman, Azim. “Advanced preclinical assessment of hyper-nociception.” 2020. Thesis, University of Adelaide. Accessed January 28, 2021.
http://hdl.handle.net/2440/127165.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Arman, Azim. “Advanced preclinical assessment of hyper-nociception.” 2020. Web. 28 Jan 2021.
Vancouver:
Arman A. Advanced preclinical assessment of hyper-nociception. [Internet] [Thesis]. University of Adelaide; 2020. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2440/127165.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Arman A. Advanced preclinical assessment of hyper-nociception. [Thesis]. University of Adelaide; 2020. Available from: http://hdl.handle.net/2440/127165
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of New South Wales
9.
Perera, Hettiarachchige.
Immunomodulatory approaches for the treatment of neuropathic pain in animal models.
Degree: Medical Sciences, 2016, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/56718
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:41227/SOURCE02?view=true
► Neuropathic pain occurring as a consequence of a disease or lesion in the somatosensory nervous system is devastating and refractory to current treatments. Neuropathic pain…
(more)
▼ Neuropathic pain occurring as a consequence of a disease or lesion in the somatosensory nervous system is devastating and refractory to current treatments.
Neuropathic pain negatively affects the quality of life of patients and causes an economic burden to the sufferers and the global economy. Thus, there is an overwhelming need to investigate the underlying mechanisms and develop novel treatment approaches. Over the past decade, it has become clear that neuroinflammation plays a critical role in the pathogenesis of
neuropathic pain. Indeed, the contribution of leukocytes such as T cells and macrophages, immune-like glial cells such as microglia and astrocytes, and inflammatory cytokines have been implicated in
neuropathic pain caused by nervous system injury. Modification of such neuroinflammatory responses via immunomodulation is a potential novel therapeutic approach for the treatment of
neuropathic pain.Myelin-derived altered peptide ligands (APLs) generated by transforming the amino acid sequence of native myelin peptides are known to modify immune and inflammatory responses, and are able to inhibit antigen-specific T cell function. APLs have demonstrated promising therapeutic effects in several in vivo and in vitro assays by changing the activation and functions of immune cells, and altering their cytokine profiles. In this thesis, we found that immunisation with the native myelin basic protein (MBP) peptide produced
pain hypersensitivity and neuroinflammation in uninjured animals and that co-immunisation with the relevant APL reduced these effects. Next, we showed that immunisation with MBP-derived APL in animals with peripheral nerve injury significantly attenuated
pain hypersensitivity and suppressed neuroinflammation, as well as altered some systemic immune responses. However, the same immunisation strategy failed to exert an analgesic effect following spinal cord injury. Lastly, the effects of gene therapy to introduce the anti-inflammatory cytokine interleukin (IL)-35 in the spinal cord were investigated in a mouse model of
neuropathic pain. We found that intrathecal administration of a plasmid DNA encoding IL-35 significantly attenuated spinal microglia activation without ameliorating
pain hypersensitivity in nerve-injured mice. These findings demonstrate the differential effects of various immunomodulatory approaches and provide important insights into the complexity of immunotherapy for the treatment of diverse
neuropathic pain conditions.
Advisors/Committee Members: Moalem-Taylor, Gila, Medical Sciences, Faculty of Medicine, UNSW, Carrive, Pascal, Medical Sciences, Faculty of Medicine, UNSW.
Subjects/Keywords: Immunomodulation; Neuropathic pain; Neuroinflammation
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APA (6th Edition):
Perera, H. (2016). Immunomodulatory approaches for the treatment of neuropathic pain in animal models. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/56718 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:41227/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Perera, Hettiarachchige. “Immunomodulatory approaches for the treatment of neuropathic pain in animal models.” 2016. Doctoral Dissertation, University of New South Wales. Accessed January 28, 2021.
http://handle.unsw.edu.au/1959.4/56718 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:41227/SOURCE02?view=true.
MLA Handbook (7th Edition):
Perera, Hettiarachchige. “Immunomodulatory approaches for the treatment of neuropathic pain in animal models.” 2016. Web. 28 Jan 2021.
Vancouver:
Perera H. Immunomodulatory approaches for the treatment of neuropathic pain in animal models. [Internet] [Doctoral dissertation]. University of New South Wales; 2016. [cited 2021 Jan 28].
Available from: http://handle.unsw.edu.au/1959.4/56718 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:41227/SOURCE02?view=true.
Council of Science Editors:
Perera H. Immunomodulatory approaches for the treatment of neuropathic pain in animal models. [Doctoral Dissertation]. University of New South Wales; 2016. Available from: http://handle.unsw.edu.au/1959.4/56718 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:41227/SOURCE02?view=true
University of Debrecen
10.
Malka, Reut.
Pharmacological treatment of neuropathic pain
.
Degree: DE – Általános Orvostudományi Kar, University of Debrecen
URL: http://hdl.handle.net/2437/220854
Subjects/Keywords: neuropathic pain;
pathophysiology
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Malka, R. (n.d.). Pharmacological treatment of neuropathic pain
. (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/220854
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Malka, Reut. “Pharmacological treatment of neuropathic pain
.” Thesis, University of Debrecen. Accessed January 28, 2021.
http://hdl.handle.net/2437/220854.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Malka, Reut. “Pharmacological treatment of neuropathic pain
.” Web. 28 Jan 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Malka R. Pharmacological treatment of neuropathic pain
. [Internet] [Thesis]. University of Debrecen; [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2437/220854.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
Malka R. Pharmacological treatment of neuropathic pain
. [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/220854
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
University of Manitoba
11.
Urban, Lawrence Michael.
The slump test, a screening tool for neuropathic pain.
Degree: Medical Rehabilitation, 2011, University of Manitoba
URL: http://hdl.handle.net/1993/4833
► This study investigated the utility of using a neurodynamic test, the Slump test by itself and with qualifiers to identify neuropathic pain (NeP). The study…
(more)
▼ This study investigated the utility of using a neurodynamic test, the Slump test by itself and with qualifiers to identify
neuropathic pain (NeP).
The study utilized a control group and a low back
pain group. The low back
pain group was pre-diagnosed as NeP or non
neuropathic pain (NNP) by an experienced clinician using an accepted diagnostic examination. A slump test was performed recording knee ROM,
pain location and verbal
pain descriptors followed by Quantitative Sensory Testing (QST).
Various versions of the slump test were compared to the pre test diagnosis. Sensitivity, specificity and likelihood ratios were calculated. The conventional slump test was shown to be a sensitive and moderately specific screening test for NeP. Including whether
pain extended below the knee dramatically increased specificity.
QST revealed localized cold sensation hyposensitivity, widespread cold
pain hyposensitivity and suggestions of increased thresholds of pressure
pain levels.
Advisors/Committee Members: MacNeil, Brian (Medical Rehabilitation) (supervisor), Shay, Barbara (Medical Rehabilitation) Schmidt, Brian (Internal Medicine (Neurology) & Physiology) (examiningcommittee).
Subjects/Keywords: slump test; neuropathic pain; neurodynamic testing
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APA (6th Edition):
Urban, L. M. (2011). The slump test, a screening tool for neuropathic pain. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4833
Chicago Manual of Style (16th Edition):
Urban, Lawrence Michael. “The slump test, a screening tool for neuropathic pain.” 2011. Masters Thesis, University of Manitoba. Accessed January 28, 2021.
http://hdl.handle.net/1993/4833.
MLA Handbook (7th Edition):
Urban, Lawrence Michael. “The slump test, a screening tool for neuropathic pain.” 2011. Web. 28 Jan 2021.
Vancouver:
Urban LM. The slump test, a screening tool for neuropathic pain. [Internet] [Masters thesis]. University of Manitoba; 2011. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1993/4833.
Council of Science Editors:
Urban LM. The slump test, a screening tool for neuropathic pain. [Masters Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4833
University of Edinburgh
12.
Medhurst, Stephen John.
Investigating the association between P2X7 receptors, microglia and the actions of morphine.
Degree: PhD, 2011, University of Edinburgh
URL: http://hdl.handle.net/1842/5539
► P2X7 receptors belong to a family of membrane bound ion channels which are activated by extracellular ATP, resulting in the opening of a non-selective cation…
(more)
▼ P2X7 receptors belong to a family of membrane bound ion channels which are activated by extracellular ATP, resulting in the opening of a non-selective cation channel. After prolonged or repeated exposure to agonist, functional and cellular changes can occur, including the formation of a large pore, cell lysis and the release of mature, biologically active interleukin-1β. It is this diversity of functions that underlies the significance of this receptor in pain processing. P2X7 receptors are expressed on microglia, which when activated, release a host of mediators which contribute to central sensitisation, a phenomenon associated with neuropathic pain. The role of P2X7 receptors in the activation of microglia is less well established and is the main subject of this thesis. Before considering the interaction between P2X7 receptors and microglia, the first aim was to establish whether P2X7 receptors played a role in a pathological process known to be associated with microglial activation. An additional aim was to establish whether the site of action was in the central nervous system (CNS), where microglia are located. These aims were accomplished using a surgery-based rat model of neuropathic pain, the chronic constriction injury (CCI) model, and by comparing the effects of different P2X7 receptor antagonists when dosed peripherally or directly into the spinal cord. The results indicated that P2X7 receptor antagonists produced efficacy in the CCI model via a mechanism located in the CNS. To further investigate the association between P2X7 receptors and microglia, a different experimental paradigm was explored. Chronically dosed morphine is known to activate microglia, the consequence of which is thought to underlie morphine tolerance and reduced morphine analgesia. By administering a P2X7 receptor antagonist to CCI-operated rats treated with chronic morphine, the interaction between the P2X7 receptor and morphine tolerance and analgesia was explored. The results showed that P2X7 receptor antagonism delayed morphine tolerance and increased the efficacy of low doses of morphine, suggesting an association between P2X7 receptors and microglia. It was intended to confirm the interaction between a P2X7 receptor antagonist and morphine in another neuropathic pain model, namely varicella zoster virus-induced neuropathy. However due to a lack of reproducibility, this model was not used for pharmacological studies. Having demonstrated an association between P2X7 receptor antagonist and morphine in a chronic pain setting, studies were initiated to explore whether this interaction occurred in other morphine-related behaviours. The effect on body weight, motor coordination and single dosed morphine-induced analgesia was assessed in rats co-administered with P2X7 receptor antagonist and morphine. Results demonstrated that the blockade of P2X7 receptors enhanced morphine acute dose-induced analgesia, but had no influence on motor-impairment and body weight. The final part of the thesis used immunohistochemical and molecular techniques…
Subjects/Keywords: 616.8; P2X7; receptors; microglia; morphine; neuropathic pain
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APA ·
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Manager
APA (6th Edition):
Medhurst, S. J. (2011). Investigating the association between P2X7 receptors, microglia and the actions of morphine. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/5539
Chicago Manual of Style (16th Edition):
Medhurst, Stephen John. “Investigating the association between P2X7 receptors, microglia and the actions of morphine.” 2011. Doctoral Dissertation, University of Edinburgh. Accessed January 28, 2021.
http://hdl.handle.net/1842/5539.
MLA Handbook (7th Edition):
Medhurst, Stephen John. “Investigating the association between P2X7 receptors, microglia and the actions of morphine.” 2011. Web. 28 Jan 2021.
Vancouver:
Medhurst SJ. Investigating the association between P2X7 receptors, microglia and the actions of morphine. [Internet] [Doctoral dissertation]. University of Edinburgh; 2011. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1842/5539.
Council of Science Editors:
Medhurst SJ. Investigating the association between P2X7 receptors, microglia and the actions of morphine. [Doctoral Dissertation]. University of Edinburgh; 2011. Available from: http://hdl.handle.net/1842/5539
Queens University
13.
Holdridge, Sarah.
Investigating the Effects of Peripheral Nerve Injury on δ Opioid Receptor Expression and Function: Implications for the Treatment of Chronic Neuropathic Pain
.
Degree: Pharmacology and Toxicology, 2009, Queens University
URL: http://hdl.handle.net/1974/1762
► Neuropathic (NP) pain is a debilitating chronic pain disorder that is a challenge to diagnose and an even greater challenge to treat. Commonly described as…
(more)
▼ Neuropathic (NP) pain is a debilitating chronic pain disorder that is a challenge to diagnose and an even greater challenge to treat. Commonly described as burning or shock-like, NP pain is characteristically resistant to traditional analgesic therapy. This thesis project aimed to investigate the potential therapeutic benefit of delta opioid receptor (δOR)-selective agonists in the management of NP pain. In the current experiments, rats that underwent unilateral sciatic nerve injury displayed characteristic behavioural manifestations including cold and thermal hyperalgesia as well as tactile allodynia in the ipsilateral hind paw. The spinal administration of DLT, a δOR-selective agonist, dose-dependently reversed tactile allodynia in NP rats and attenuated cold and thermal hypersensitivities. Moreover, DLT produced greater antinociceptive effects in NP rats compared with controls in the cold water paw withdrawal, hot water tail flick, and thermal plantar box tests. Nerve injury-induced augmentation in δOR function was dependent on nociceptive afferents, since the effect was absent in NP rats that received neonatal treatment with capsaicin. Furthermore, it was not due to increased δOR biosynthesis as western blots and immunohistochemistry revealed no change in spinal δOR protein. We hypothesized that an alternative mechanism, such as redistribution of receptors within the neuron, may underlie δOR function changes. Using immunogold electron microscopy, we showed that nerve injury indeed increased the cell surface expression of δORs within dendritic profiles of the dorsal horn via redistribution of existing receptors. Interestingly, this event was observed bilaterally in the deep dorsal horn, with no effect in the superficial laminae. The mechanisms underlying nerve injury-induced δOR trafficking remain unclear however we may take cues from other δOR trafficking events. We showed that concomitant treatment of rats with morphine and a glial inhibitor prevented both the activation of spinal glia and the changes in δOR agonist effects observed with morphine alone, suggesting that glial activity contributes to morphine-induced δOR trafficking in vivo and may provide insight into the mechanisms underlying nerve injury-induced δOR trafficking. Collectively, these studies reveal an important role of δORs in modulating pain symptoms associated with nerve injury, supporting further exploration of δORs as novel therapeutic targets in the treatment of NP pain.
Subjects/Keywords: Opioid
;
Neuropathic Pain
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Holdridge, S. (2009). Investigating the Effects of Peripheral Nerve Injury on δ Opioid Receptor Expression and Function: Implications for the Treatment of Chronic Neuropathic Pain
. (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/1762
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Holdridge, Sarah. “Investigating the Effects of Peripheral Nerve Injury on δ Opioid Receptor Expression and Function: Implications for the Treatment of Chronic Neuropathic Pain
.” 2009. Thesis, Queens University. Accessed January 28, 2021.
http://hdl.handle.net/1974/1762.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Holdridge, Sarah. “Investigating the Effects of Peripheral Nerve Injury on δ Opioid Receptor Expression and Function: Implications for the Treatment of Chronic Neuropathic Pain
.” 2009. Web. 28 Jan 2021.
Vancouver:
Holdridge S. Investigating the Effects of Peripheral Nerve Injury on δ Opioid Receptor Expression and Function: Implications for the Treatment of Chronic Neuropathic Pain
. [Internet] [Thesis]. Queens University; 2009. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1974/1762.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Holdridge S. Investigating the Effects of Peripheral Nerve Injury on δ Opioid Receptor Expression and Function: Implications for the Treatment of Chronic Neuropathic Pain
. [Thesis]. Queens University; 2009. Available from: http://hdl.handle.net/1974/1762
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
14.
Alshelh, Zeynab.
Infra-slow oscillations in chronic orofacial neuropathic pain and the effects of palmitoylethanolamide
.
Degree: 2018, University of Sydney
URL: http://hdl.handle.net/2123/18655
► For centuries, chronic pain was denied as being real by physicians, mainly because there was no evidence of tissue damage. The lack of understanding of…
(more)
▼ For centuries, chronic pain was denied as being real by physicians, mainly because there was no evidence of tissue damage. The lack of understanding of the neural mechanisms underlying chronic pain, particular that arising from nervous system damage, has hindered treatment development which has led to the over-prescription of opioids. Whilst the brain circuitry responsible for the perception of acute painful stimuli have been mapped in both animal studies and studies using brain imaging in awake humans, the circuitry responsible for the initiation and maintenance of chronic pain remain unknown. Over the past few decades, many human brain imaging investigations have shown that neuropathic pain is associated with altered brain rhythms and in particular thalamocortical dysrhythmia. In addition, animal studies have shown that neuropathic pain is associated with altered non-neural function including microglial and astrocyte activation at the level of the primary afferent synapse. These results have led to theories that non-neuronal cells may be crucial for the initiation and maintenance of chronic pain, particularly chronic neuropathic pain. It has been a long held view that astrocytes mainly play the role of neural support in the central nervous system, however, these cells are also capable of controlling neural function. In fact, astrocytes have access to every neural synapse and animal models of chronic neuropathic pain have shown that targeting astrocytes can control pain intensity. As such, the focus of this thesis is to identify the role of astrocytes in modulating neural function in chronic neuropathic pain and to determine whether reducing astrocyte activity can reduce pain intensity. There are three main investigations that make up this thesis, the first describes an experimental procedure whereby on-going patterns of neural activity were assessed in patients with orofacial neuropathic pain using resting state functional magnetic resonance imaging. The second attempts to measure an anatomical marker of astrocyte activation. And the final investigation describes an experimental procedure whereby patients with orofacial neuropathic pain were administered an astrocyte modulator, palmitoylethanolamide (PEA) and neural activity was compared before and after treatment.
Subjects/Keywords: Palmitoylethanolamide;
chronic pain;
neuropathic;
T2 relaxometry
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APA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Alshelh, Z. (2018). Infra-slow oscillations in chronic orofacial neuropathic pain and the effects of palmitoylethanolamide
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/18655
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Alshelh, Zeynab. “Infra-slow oscillations in chronic orofacial neuropathic pain and the effects of palmitoylethanolamide
.” 2018. Thesis, University of Sydney. Accessed January 28, 2021.
http://hdl.handle.net/2123/18655.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Alshelh, Zeynab. “Infra-slow oscillations in chronic orofacial neuropathic pain and the effects of palmitoylethanolamide
.” 2018. Web. 28 Jan 2021.
Vancouver:
Alshelh Z. Infra-slow oscillations in chronic orofacial neuropathic pain and the effects of palmitoylethanolamide
. [Internet] [Thesis]. University of Sydney; 2018. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2123/18655.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Alshelh Z. Infra-slow oscillations in chronic orofacial neuropathic pain and the effects of palmitoylethanolamide
. [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/18655
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
15.
Manion, John William.
The Conserved Genetic Architecture of Pain
.
Degree: University of Sydney
URL: http://hdl.handle.net/2123/21746
► Evolutionary models such as Drosophila have proved powerful for the interrogation of many peripheral nervous disorders including in motor neuron disease and pain. Given the…
(more)
▼ Evolutionary models such as Drosophila have proved powerful for the interrogation of many peripheral nervous disorders including in motor neuron disease and pain. Given the evolutionary conservation of the peripheral nervous system, model organisms provide a powerful tool for the investigation of pain. Here we demonstrate several vignettes that show firstly, how relatively simple organisms can provide rapid models to assess and understand Mendelian disorders. We then show how simple models can be interrogated to identify central druggable pathways to develop a new stem cell therapy. Finally, we utilise the evolutionary conservation between mammalian species to validate developmental pathways and apply these to a therapeutic context. We apply this approach to a significant problem, pain. Throughout this thesis we apply new technologies to identify potentially druggable pathways and utilise simple organisms to test and validate them. Through our literature review, we firstly provide an overview of the central knowledge of pain perception, chronic pain, approaches to its treatment, the genetic basis of rare pain disorders and finally approaches to modelling pain. Secondly, we approach epigenetics, and assess the central mechanisms of epigenetics followed by an assessment of its role in pain perception.
Subjects/Keywords: Neuropathic;
GABAergic;
Pain
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Manion, J. W. (n.d.). The Conserved Genetic Architecture of Pain
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/21746
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Manion, John William. “The Conserved Genetic Architecture of Pain
.” Thesis, University of Sydney. Accessed January 28, 2021.
http://hdl.handle.net/2123/21746.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Manion, John William. “The Conserved Genetic Architecture of Pain
.” Web. 28 Jan 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Manion JW. The Conserved Genetic Architecture of Pain
. [Internet] [Thesis]. University of Sydney; [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2123/21746.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
Manion JW. The Conserved Genetic Architecture of Pain
. [Thesis]. University of Sydney; Available from: http://hdl.handle.net/2123/21746
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
University of New South Wales
16.
Abdulla, Munawwar.
Investigating neuroprotectants for the treatment of Chemotherapy-Induced Peripheral Neuropathy.
Degree: Medical Sciences, 2018, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/60359
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51899/SOURCE02?view=true
► Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating and dose-limiting side effect of many chemotherapy regimens and is becoming a more prevalent issue as the longevity…
(more)
▼ Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating and dose-limiting side effect of many chemotherapy regimens and is becoming a more prevalent issue as the longevity of cancer patients continues to increase. Sensory symptoms include
neuropathic pain, paraesthesia, and numbness and usually spread in a glove-and-stocking distribution. At present, there are no effective medications to treat or prevent CIPN, and the mechanisms by which symptoms are induced have not been fully elucidated. Paclitaxel (PTX) is a commonly used chemotherapeutic that induces neuropathy in a high percentage of patients. The broad aim of this thesis was to establish a model of CIPN in vitro and in vivo and test clinically approved drugs for potential neuroprotective effects. Since the dorsal root ganglion (DRG) has been implicated in CIPN, we cultured dissociated primary DRG neurons from 5-week-old C57BL/6 mice and treated them with PTX to observe neurotoxic effects. We found a marked reduction of neurite outgrowth per neuron and significant morphological changes. Next, we tested several drugs selected from the literature (ibudilast, nicotinamide mononucleotide, resatorvid, amiloride, duloxetine, safinamide) for their potential neuroprotective effects in this model and of those, found that amiloride moderately but significantly prevented the reduction of neurite outgrowth at a certain concentration, although could be harmful if the concentration was too high. We then established a chronic CIPN model in C57BL/6 mice using 6 injections of PTX over a two-week period. PTX-treated mice developed mechanical allodynia, an increase in acetylated tubulin representing damage in the sciatic nerve, increased macrophage presence in the DRG and increased glial cell activation in the spinal cord. Amiloride given at 5 mg/kg, 2 hrs before each PTX treatment was found to have moderate but significant effect in ameliorating mechanical allodynia and reducing astrogliosis in the spinal cord. Taken together, the experiments in this thesis provide in vitro and in vivo models to test drugs against PTX-induced neurotoxicity and present some evidence of amiloride’s potential use to treat PTX-induced peripheral neuropathy. However, further work is required to understand the mechanisms underlying amiloride effects in CIPN, and its drug safety profile in models of cancer.
Advisors/Committee Members: Moalem-Taylor, Gila, Medical Sciences, Faculty of Medicine, UNSW, Lees, Justin, Medical Sciences, Faculty of Medicine, UNSW, Pollie, Patsie, Medical Sciences, Faculty of Medicine, UNSW.
Subjects/Keywords: Neuropathic pain; CIPN; Amiloride; Paclitaxel; Chemotherapy
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Abdulla, M. (2018). Investigating neuroprotectants for the treatment of Chemotherapy-Induced Peripheral Neuropathy. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/60359 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51899/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Abdulla, Munawwar. “Investigating neuroprotectants for the treatment of Chemotherapy-Induced Peripheral Neuropathy.” 2018. Masters Thesis, University of New South Wales. Accessed January 28, 2021.
http://handle.unsw.edu.au/1959.4/60359 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51899/SOURCE02?view=true.
MLA Handbook (7th Edition):
Abdulla, Munawwar. “Investigating neuroprotectants for the treatment of Chemotherapy-Induced Peripheral Neuropathy.” 2018. Web. 28 Jan 2021.
Vancouver:
Abdulla M. Investigating neuroprotectants for the treatment of Chemotherapy-Induced Peripheral Neuropathy. [Internet] [Masters thesis]. University of New South Wales; 2018. [cited 2021 Jan 28].
Available from: http://handle.unsw.edu.au/1959.4/60359 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51899/SOURCE02?view=true.
Council of Science Editors:
Abdulla M. Investigating neuroprotectants for the treatment of Chemotherapy-Induced Peripheral Neuropathy. [Masters Thesis]. University of New South Wales; 2018. Available from: http://handle.unsw.edu.au/1959.4/60359 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51899/SOURCE02?view=true
Virginia Tech
17.
Bustamante Diaz, Hedie A.
The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats.
Degree: PhD, Veterinary Medical Sciences, 2011, Virginia Tech
URL: http://hdl.handle.net/10919/77103
► Satellite glial cells (SGC) are laminar cells that wrap completely around the sensory neuron and are responsible for buffering extracellular K+ after neuronal excitation. A…
(more)
▼ Satellite glial cells (SGC) are laminar cells that wrap completely around the sensory neuron and are responsible for buffering extracellular K+ after neuronal excitation. A decrease in the potassium buffering capacity of SGC has been associated with
neuropathic pain (NP) behavior and apoptosis. This dissertation investigated the role of the potassium buffering capacity and apoptosis of trigeminal satellite glial cells (SGC) in the maintenance and development of orofacial NP in rats using in vivo and in vitro methodologies. In vivo endpoints were evaluated after performing chronic constriction injury (CCI) of the infraorbital nerve (IoN). NP signs and behavior were evaluated at 5, 10, 20 40 and 80 hours after injury. We evaluated the potassium buffering capacity of SGC by measuring the intracellular potassium concentration and protein levels and gene expression of the Kir4.1 and the SK3 potassium channels and gap junction protein connexin 43 (Cx43). We evaluated apoptosis endpoints including protein levels and gene expression of apoptotic related proteins bcl-2, caspase 9, caspase 3 and p53. Results indicate that NP signs developed as early as 5 hours after injury. After PNI, SGC responded by increasing their intracellular potassium concentration and by increasing protein levels of Kir4.1, SK3 and Cx43. Nonetheless, this increase in protein levels was not accompanied by an increase in gene expression. Apoptosis results revealed that SGC decreased protein levels and gene expression of anti-apoptotic protein Bcl-2. Using in vitro methodologies, we developed primary trigeminal SGC cultures and evaluated how a decrease in the intracellular potassium concentration modulates apoptosis induced by the mitochondrial and death receptor pathways. SGC depleted of potassium after hypoosmotic shock showed a significant increase in early apoptosis after incubation with mitochondrial pathway apoptotic inducer staurosporine when compared to SGC with normal intracellular concentration. This research has revealed that SGC respond early to PNI by increasing their potassium buffering capacity. We also determined that the mitochondrial apoptotic pathway might be involved in the trigeminal SGC response to PNI. From our in vitro experiments we have revealed that potassium is an important modulator of apoptosis induced by the mitochondrial pathway in cultured trigeminal SGC.
Advisors/Committee Members: Klein, Bradley G. (committeechair), Jortner, Bernard S. (committee member), Rossmeisl, John H. Jr. (committee member), Ehrich, Marion F. (committeecochair).
Subjects/Keywords: neuropathic pain; Satellite glial cells; potassium; apoptosis
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APA (6th Edition):
Bustamante Diaz, H. A. (2011). The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/77103
Chicago Manual of Style (16th Edition):
Bustamante Diaz, Hedie A. “The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats.” 2011. Doctoral Dissertation, Virginia Tech. Accessed January 28, 2021.
http://hdl.handle.net/10919/77103.
MLA Handbook (7th Edition):
Bustamante Diaz, Hedie A. “The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats.” 2011. Web. 28 Jan 2021.
Vancouver:
Bustamante Diaz HA. The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats. [Internet] [Doctoral dissertation]. Virginia Tech; 2011. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/10919/77103.
Council of Science Editors:
Bustamante Diaz HA. The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats. [Doctoral Dissertation]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/77103
University of Toronto
18.
Acland, Erinn L.
The Effect of Peripheral Nerve-injury on Depression and Anxiety-like Behaviours in Mice.
Degree: 2017, University of Toronto
URL: http://hdl.handle.net/1807/77663
► Past animal studies examining the relationship between depression and chronic pain have used only male rodents and often only assessed behaviours 7 to 14 days…
(more)
▼ Past animal studies examining the relationship between depression and chronic pain have used only male rodents and often only assessed behaviours 7 to 14 days after an injury. To determine whether chronic pain results in a sexually dimorphic presentation of depression-like behaviours, I conducted a series of experiments assessing male and female mice at 14, 28, and 42 days after a peripheral nerve injury. I found that mice did not show any changes in behaviours 14 or 28 days. At 42 days post-surgery male mice with a nerve injury showed significantly more depressive-like behaviours than the sham group, however females did not. This suggest that results from male rodents may not be generalizable to females and that studies assessing mental health and chronic pain in rodents should assess behaviour over longer periods of time as to be more representative of long-term pain experiences.
M.A.
Advisors/Committee Members: Martin, Loren J, Psychology.
Subjects/Keywords: Anxiety; Chronic Pain; Depression; Mice; Neuropathic Pain; Sex Differences; 0621
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APA ·
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APA (6th Edition):
Acland, E. L. (2017). The Effect of Peripheral Nerve-injury on Depression and Anxiety-like Behaviours in Mice. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/77663
Chicago Manual of Style (16th Edition):
Acland, Erinn L. “The Effect of Peripheral Nerve-injury on Depression and Anxiety-like Behaviours in Mice.” 2017. Masters Thesis, University of Toronto. Accessed January 28, 2021.
http://hdl.handle.net/1807/77663.
MLA Handbook (7th Edition):
Acland, Erinn L. “The Effect of Peripheral Nerve-injury on Depression and Anxiety-like Behaviours in Mice.” 2017. Web. 28 Jan 2021.
Vancouver:
Acland EL. The Effect of Peripheral Nerve-injury on Depression and Anxiety-like Behaviours in Mice. [Internet] [Masters thesis]. University of Toronto; 2017. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1807/77663.
Council of Science Editors:
Acland EL. The Effect of Peripheral Nerve-injury on Depression and Anxiety-like Behaviours in Mice. [Masters Thesis]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/77663
19.
엄, 영인.
Chronic Pain after Non-traumatic, Non-compressive Myelopathy: Characteristics and Predictors for Neuropathic pain.
Degree: 2015, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/11843
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019496
► Introduction: Chronic pain is one of the most common and serious consequences of myelopathy. The aim of this study was to survey chronic pain experience…
(more)
▼ Introduction: Chronic pain is one of the most common and serious consequences of myelopathy. The aim of this study was to survey chronic pain experience in a neurology out-patient clinic and to determine potential predictors for neuropathic pain after non-traumatic, non-compressive(NTNC) myelopathy.
Methods: We analyzed54 patients with a history of NTNC myelopathy at the neurology out-patient clinic. All patients completed questionnaires on pain severity, descriptors and impact on quality of life (QOL) and underwent neurologic examination with bedside sensory testing. The Short Form McGill Pain Questionnaire (SF-MPQ) and the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) were used to assess pain. Neuropathic pain was diagnosed by LANSS score of 12 or more. Health-related QOL was evaluated by the Short Form 36-item (SF-36) health survey, while Hospital Anxiety and Depression Scale (HADS) and Patient Global Impression of Change (PGIC) were utilized to evaluate emotion and response to treatment for pain, respectively.
Results: Out of 54 patients, 48 reported pain; of these, 41 (85.4%) reported the initiation of pain during the first 3 months of myelopathy onset. The median (min-max) pain duration and SF-MPQ score was 41 (3.4-166) months and 10 (1-34), respectively. Thirty five (72.9%) patients reported continuous pain throughout the day. The most common pain descriptions were exhausting, gnawing and heavy. In total, 16 (33.3%) patients experienced neuropathic pain. Mean age was statistically significantly lower in patients with neuropathic pain than in patients with non-neuropathic pain (39.1 ± 12.5 vs. 49.8 ± 9.3, P = 0.002). A binary logistic regression revealed that onset age under 40, non-idiopathic etiologysuch as neuromyelitis optica, multiple sclerosis were independent predictors of the occurrence of neuropathic pain. Both SF-MPQ and LANSS scores were significantly correlated with SF-36 scores, adjusted by age, sex, presence of diabetes mellitus, and current EDSS scores (r = –0.624, P< 0.0001 for SF-MPQ; r = -0.357, P = 0.017 for LANSS). Patients who showed clinical improvement (PGIC scores >2) with treatment were female, non-idiopathic etiology or lengthy lesion (> 3 vertebral segments). But the presence of diabetes was related to a poor treatment response.
Conclusion: Chronic pain is one of annoying complications in patients with NTNC myelopathy and also affects their quality of life. Onset age and etiology of myelopathyare important factors in the development of neuropathic pain in NTNC myelopathy. Pain relief research is expected to improve health-related QOL in these patients.
ABSTRACT ⅰ
TABLE OF CONTENTS ⅲ
LIST OF FIGURES ⅳ
LIST OF TABLES ⅴ
Ⅰ. INTRODUCTION 1
Ⅱ. MATERIAL AND METHOD 3
A. SUBJECTS 3
B. MYELOPATHY CHARACTERISTICS 3
C. PAIN ASSESSMENT 3
D. ASSESSMENT OF FUNCTIONAL AND EMOTIONAL STATUS 4
E. PAIN RESPONSE TO TREATMENT 4
F. STATISTICAL ANALYSIS 5
Ⅲ. RESULTS 6
A. GENERAL CHARACTERISTICS OF SUBJECTS WITH NON-TRAUMATIC, NON-COMPRESSIVE MYELOPATHY 6
B.…
Advisors/Committee Members: 대학원 의학과, 201224108, 엄, 영인.
Subjects/Keywords: Chronic pain; Non-traumatic Non-conpressive myelopathy; Neuropathic pain; Predictors
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APA (6th Edition):
엄, . (2015). Chronic Pain after Non-traumatic, Non-compressive Myelopathy: Characteristics and Predictors for Neuropathic pain. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/11843 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019496
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
엄, 영인. “Chronic Pain after Non-traumatic, Non-compressive Myelopathy: Characteristics and Predictors for Neuropathic pain.” 2015. Thesis, Ajou University. Accessed January 28, 2021.
http://repository.ajou.ac.kr/handle/201003/11843 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019496.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
엄, 영인. “Chronic Pain after Non-traumatic, Non-compressive Myelopathy: Characteristics and Predictors for Neuropathic pain.” 2015. Web. 28 Jan 2021.
Vancouver:
엄 . Chronic Pain after Non-traumatic, Non-compressive Myelopathy: Characteristics and Predictors for Neuropathic pain. [Internet] [Thesis]. Ajou University; 2015. [cited 2021 Jan 28].
Available from: http://repository.ajou.ac.kr/handle/201003/11843 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019496.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
엄 . Chronic Pain after Non-traumatic, Non-compressive Myelopathy: Characteristics and Predictors for Neuropathic pain. [Thesis]. Ajou University; 2015. Available from: http://repository.ajou.ac.kr/handle/201003/11843 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019496
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Georgia Tech
20.
Idlett Ali, Shaquia L.
Investigations of spontaneous pain and modulation with spinal cord stimulation.
Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2020, Georgia Tech
URL: http://hdl.handle.net/1853/62801
► Chronic pain is the leading cause of long-term disability. Heterogeneity in etiology and manifestation of neuropathic pain contribute to difficulties finding broadly effective pain management…
(more)
▼ Chronic
pain is the leading cause of long-term disability. Heterogeneity in etiology and manifestation of
neuropathic pain contribute to difficulties finding broadly effective
pain management strategies. In cases where pharmacological treatment has failed to provide relief, epidural spinal cord stimulation (SCS) has emerged as an alternative intervention for intractable
pain. This technology has been in clinical use for over 50 years, yet efficacy rates have remained stagnant and etiology-dependent. A barrier to improved efficacy is an absence of knowledge identifying the mechanism by which SCS can selectively inhibit chronic, spontaneous
pain.
The objective of this dissertation was to generate knowledge that leads to a better understanding of both spontaneous
neuropathic pain and SCS
pain relief. To do this, I first identified links between spontaneous sensory hyperexcitability and stimulus-independent physio-behavioral indices of
pain, using a contusion model of spinal cord injury. Next, I used an ex vivo adult mouse spinal cord preparation to assess axonal recruitment with SCS. A computational model was utilized to inform parameter selection for examining clinically-analogous SCS with our model system. Finally, I tested the gate control theory by examining SCS modulation in an ex vivo model of spontaneous
pain. I employed a threshold-based approach to examine SCS modulation of spontaneous nociceptive activity using traditional frequencies of SCS. Results indicate that afferent recruitment alone is not sufficient to replicate aspects of SCS modulation observed clinically. Together, these findings provide greater insight into the identification of spontaneous
neuropathic pain and the underlying mechanisms leading to
pain relief with SCS.
Advisors/Committee Members: Hochman, Shawn (advisor).
Subjects/Keywords: Neuropathic pain; Neuromodulation; Chronic pain; Spinal cord stimulation; Spinal cord; Neurophysiology
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APA (6th Edition):
Idlett Ali, S. L. (2020). Investigations of spontaneous pain and modulation with spinal cord stimulation. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/62801
Chicago Manual of Style (16th Edition):
Idlett Ali, Shaquia L. “Investigations of spontaneous pain and modulation with spinal cord stimulation.” 2020. Doctoral Dissertation, Georgia Tech. Accessed January 28, 2021.
http://hdl.handle.net/1853/62801.
MLA Handbook (7th Edition):
Idlett Ali, Shaquia L. “Investigations of spontaneous pain and modulation with spinal cord stimulation.” 2020. Web. 28 Jan 2021.
Vancouver:
Idlett Ali SL. Investigations of spontaneous pain and modulation with spinal cord stimulation. [Internet] [Doctoral dissertation]. Georgia Tech; 2020. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1853/62801.
Council of Science Editors:
Idlett Ali SL. Investigations of spontaneous pain and modulation with spinal cord stimulation. [Doctoral Dissertation]. Georgia Tech; 2020. Available from: http://hdl.handle.net/1853/62801
University of Toronto
21.
Mapplebeck, Josiane.
Sex Differences in the Spinal Mechanisms Underlying Chronic Pain.
Degree: PhD, 2018, University of Toronto
URL: http://hdl.handle.net/1807/97897
► Microglia-neuronal signalling has been critically implicated in mediating pain hypersensitivity associated with peripheral nerve injury (PNI). PNI causes upregulation of the purinergic receptor P2X4 (P2X4R)…
(more)
▼ Microglia-neuronal signalling has been critically implicated in mediating pain hypersensitivity associated with peripheral nerve injury (PNI). PNI causes upregulation of the purinergic receptor P2X4 (P2X4R) on microglia, which elicits brain-derived neurotrophic factor release (BDNF). BDNF acts on spinal dorsal horn neurons, leading to enhancement of NMDA receptor (NMDAR) activity and downregulation of the potassium chloride cotransporter KCC2. Together, these neuronal changes cause hyperexcitability of lamina I neurons which transmit pain information to the brain. Unfortunately, the P2X4R-BDNF-NMDAR/KCC2 framework was delineated through experiments employing exclusively male rodents. This sex bias in subject inclusion is rampant in preclinical pain research. Here, we found that disrupting microglial P2X4R-BDNF signalling, which blocked pain hypersensitivity in males, had no effect in females. Thus, we concluded that microglia-neuronal signalling does not contribute to neuropathic pain hypersensitivity in female mice. Furthermore, we found that females lacking T cells, which are critical mediators of adaptive immunity, ‘switched’ to using the microglial-dependent pathway. These findings suggest that T cells may play an analogous role to microglia in females with pain hypersensitivity. Our qPCR and flow cytometry experiments indicated that this sexual dimorphism appears to be dependent on a lack of increased P2X4R activity in females after nerve injury. Additionally, we found that modulators of microglia functioning attenuated CFA-induced hypersensitivity in males only, demonstrating that a sexually dimorphic role for microglia also exists in inflammatory pain. We also demonstrated that this sex difference in pain signalling likewise occurs in rats, thus there is conservation of this phenomenon between different rodent species. Further, we showed that nerve injury downregulated KCC2 in both sexes, and pharmacologically targeting KCC2 or NMDARs rescued pain hypersensitivity in females and males. Thus, despite sexually dimorphic immune pain signalling, NMDARs and KCC2 contribute to pain hypersensitivity in both sexes. Therefore, neuronal mechanisms downstream of microglia are convergent between the sexes, which reveal that pain hypersensitivity is degenerate, in that multiple processes can lead to the same pathological change. Our findings demonstrate that future development of drug therapies for chronic pain should target non-degenerate mechanisms and highlight the importance of including female subjects in preclinical pain research.
2019-11-19 00:00:00
Advisors/Committee Members: Salter, Michael W, Physiology.
Subjects/Keywords: Chronic Pain; Microglia; Neuropathic Pain; Rodents; Sex Differences; T cells; 0317
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APA (6th Edition):
Mapplebeck, J. (2018). Sex Differences in the Spinal Mechanisms Underlying Chronic Pain. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/97897
Chicago Manual of Style (16th Edition):
Mapplebeck, Josiane. “Sex Differences in the Spinal Mechanisms Underlying Chronic Pain.” 2018. Doctoral Dissertation, University of Toronto. Accessed January 28, 2021.
http://hdl.handle.net/1807/97897.
MLA Handbook (7th Edition):
Mapplebeck, Josiane. “Sex Differences in the Spinal Mechanisms Underlying Chronic Pain.” 2018. Web. 28 Jan 2021.
Vancouver:
Mapplebeck J. Sex Differences in the Spinal Mechanisms Underlying Chronic Pain. [Internet] [Doctoral dissertation]. University of Toronto; 2018. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1807/97897.
Council of Science Editors:
Mapplebeck J. Sex Differences in the Spinal Mechanisms Underlying Chronic Pain. [Doctoral Dissertation]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/97897
University of Toronto
22.
Mashregi, Mariam Fadiah.
Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection.
Degree: PhD, 2017, University of Toronto
URL: http://hdl.handle.net/1807/92683
► Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection Mariam Mashregi Doctor of Philosophy Faculty of Dentistry University of Toronto 2017 Abstract Orofacial nerve injuries…
(more)
▼ Extraterritorial Heat Hyperalgesia in Mice Following
Infraorbital Nerve Transection
Mariam Mashregi
Doctor of Philosophy
Faculty of Dentistry
University of Toronto
2017
Abstract
Orofacial nerve injuries often lead to long-lasting pain which, is frequently perceived outside the field of injury (extraterritorial pain) and continues long after healing is complete. It has been suggested that sex and genetic factors may contribute to the development of neuropathic pain. These aspects were addressed in the present dissertation by first assessing nociceptive responses to noxious radiant heat stimuli in healthy male and female mice of the AXB-BXA recombinant inbred panel (A/J and C57BL/6J parental strains and their 23 descendant strains), and then comparing baseline responses to nociceptive responses following unilateral infraorbital nerve transection (IONX) or sham surgery, in the ears, ventral and dorsal tail, and hind-paws. These body sites were extraterritorial to the field innervated by the infraorbital nerve. Strain differences in heat hyperalgesia were utilised as phenotypes for genetic linkage analysis to identify chromosomal regions harbouring candidate genes.
Since heat absorption depends on skin pigmentation, and the 25 strains were comprised of black, agouti (light-brown/taupe), and white coat colours, a standard heat intensity that elicited a threshold withdrawal at each body site was determined for each coat colour group and used for subsequent studies.
Significant body-site-specific and strain-specific differences in baseline heat nociception were found, however, no sex differences were noted except in the ventral tail (male > female). Sensitisation to repeated noxious stimulation within the same test session was also noted in all body sites tested.
Following surgery (IONX and sham), significant heat hyperalgesia was seen in many strains in all tested body sites. Sex differences were seen only in the ventral tail (female > male). The same post-operative increases were seen in both the sham and IONX groups, which might be explained by surgery-induced neuritis.
Narrow-sense heritability estimates for baseline heat nociception and post-operative extraterritorial heat hyperalgesia ranged from 0.09 to 0.49 (in all body sites). Suggestive (but not significant) quantitative trait loci were mapped for baseline heat nociception in chromosomes 3,7,9, and 13 and for post-operative heat hyperalgesia in chromosomes 4, 11, and X. Several candidate genes were identified in these suggestive regions thus, necessitating future research to identify the causative genes.
2018-11-30 00:00:00
Advisors/Committee Members: Seltzer, Ze'ev, Dentistry.
Subjects/Keywords: Animal models; Genetics; Neuropathic pain; Neuroscience; Pain; Sensory behavioural; 0317
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APA ·
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APA (6th Edition):
Mashregi, M. F. (2017). Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/92683
Chicago Manual of Style (16th Edition):
Mashregi, Mariam Fadiah. “Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection.” 2017. Doctoral Dissertation, University of Toronto. Accessed January 28, 2021.
http://hdl.handle.net/1807/92683.
MLA Handbook (7th Edition):
Mashregi, Mariam Fadiah. “Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection.” 2017. Web. 28 Jan 2021.
Vancouver:
Mashregi MF. Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1807/92683.
Council of Science Editors:
Mashregi MF. Extraterritorial Heat Hyperalgesia in Mice Following Infraorbital Nerve Transection. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/92683
University of Minnesota
23.
Peterson, Cristina.
Alleviation of Chronic Neuropathic Pain by Agmatine Requires the GluN2B Subunit of the NMDA Receptor.
Degree: PhD, Experimental & Clinical Pharmacology, 2017, University of Minnesota
URL: http://hdl.handle.net/11299/193441
► Effective treatment for chronic pain patients remains an area of largely unmet need. However, chronic pain patients receiving traditional opioid therapy are consistently surrounded by…
(more)
▼ Effective treatment for chronic pain patients remains an area of largely unmet need. However, chronic pain patients receiving traditional opioid therapy are consistently surrounded by the potential risks and social stigmas of opioid dependence, misuse, and addiction. These concerns are heightened in the face of the expanding opioid epidemic. The need for new, non-opioidergic therapeutics for management of the large population of chronic patients is widely recognized. Agmatine, also known as decarboxylated arginine, is an endogenous small molecule that has been shown to modulate maladaptive neuroplasticity that underlies the experience of chronic pain. Agmatine has been established to meet the criteria of acting as a neurotransmitter including synthesis in neurons, release from nerve terminals, and binding to post-synaptic receptors. We have previously demonstrated the efficacy of exogenously delivered agmatine in reversing chronic pain behaviors in models of neuropathic pain. Targeting primary sensory neurons through gene vectors such as serotypes of the adeno-associated virus has recently been identified as a powerful emerging strategy to treat chronic, intractable pain. Gene therapy has been approved for market use in Europe and the United States, making it a viable tool for translation from bench side to clinic. To this end, a viral vector encoding the synthetic enzyme for agmatine, namely arginine decarboxylase was developed. It has been shown that intrathecally injected viral vector particles distribute to sites of interest for chronic pain. The primary objective of my thesis work has been to expand both the application and mechanistic understanding of agmatine as a non-opioidergic therapeutic in the treatment of chronic pain. The central hypothesis of this work is that enhanced expression of arginine decarboxylase in nociceptive pathways results in long-term reduction of neuropathic pain due to agmatine production and agmatine’s antagonism of the NMDA receptor. The rationale for this research was that delivery of a gene therapy to enhance agmatine’s inhibition of NMDA signaling would be a viable, long term solution for management of chronic pain. In this thesis, I will expand upon the dual public health crises of chronic pain and prescription opioid abuse. These call for new, non-opioid therapeutic approaches for chronic pain, leading to the therapeutic development of agmatine as an NMDA receptor antagonist.
Subjects/Keywords: Agmatine; Chronic Pain; Gene Therapy; GluN2B; Neuropathic Pain; NMDA Receptor
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APA (6th Edition):
Peterson, C. (2017). Alleviation of Chronic Neuropathic Pain by Agmatine Requires the GluN2B Subunit of the NMDA Receptor. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/193441
Chicago Manual of Style (16th Edition):
Peterson, Cristina. “Alleviation of Chronic Neuropathic Pain by Agmatine Requires the GluN2B Subunit of the NMDA Receptor.” 2017. Doctoral Dissertation, University of Minnesota. Accessed January 28, 2021.
http://hdl.handle.net/11299/193441.
MLA Handbook (7th Edition):
Peterson, Cristina. “Alleviation of Chronic Neuropathic Pain by Agmatine Requires the GluN2B Subunit of the NMDA Receptor.” 2017. Web. 28 Jan 2021.
Vancouver:
Peterson C. Alleviation of Chronic Neuropathic Pain by Agmatine Requires the GluN2B Subunit of the NMDA Receptor. [Internet] [Doctoral dissertation]. University of Minnesota; 2017. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/11299/193441.
Council of Science Editors:
Peterson C. Alleviation of Chronic Neuropathic Pain by Agmatine Requires the GluN2B Subunit of the NMDA Receptor. [Doctoral Dissertation]. University of Minnesota; 2017. Available from: http://hdl.handle.net/11299/193441
24.
Pommier, Benjamin.
Neurostimulations du cortex moteur ou d’ailleurs, invasives ou non, dans la douleur centrale : Cortical neurostimulations, both invasive and non-invasive, to treat central neuropathic pain.
Degree: Docteur es, Neurosciences, 2019, Lyon
URL: http://www.theses.fr/2019LYSES009
► La douleur neuropathique centrale est une affection fréquente dont le traitement est complexe. En raison d’un important taux de résistance aux traitements pharmacologiques, des techniques…
(more)
▼ La douleur neuropathique centrale est une affection fréquente dont le traitement est complexe. En raison d’un important taux de résistance aux traitements pharmacologiques, des techniques de neuromodulation ont été développées. Parmi elles, on retrouve les stimulations du cortex moteur primaire (ou gyrus précentral), invasive (i.e. stimulation électrique épidurale, eMCS) et non-invasive (i.e. stimulation magnétique transcrânienne répétitive, rTMS). Ces techniques restent limitées par différents paramètres. La rTMS a principalement été étudiée à travers des séances uniques, et son efficacité comme moyen thérapeutique au long cours reste mal connue. La eMCS souffre d’un manque de prédicteurs individuels d’efficacité suffisamment robustes pour sélectionner à bon escient les candidats à la chirurgie. Enfin, le cortex moteur primaire est une cible de découverte empirique, et d’autres cibles sont à envisager pour améliorer les résultats de ces neuromodulations corticales. Notre travail avait pour objectif l’amélioration des connaissances vis à vis de ces différentes limites. Il s’est articulé autour de 3 axes principaux :- L’étude de la rTMS en séances répétées, au long cours, comme moyen thérapeutique à part entière. - L’étude de la rTMS en séances répétées comme moyen de prédiction de la réponse antalgique à la eMCS.- Le développement de méthodes permettant la localisation fiable et reproductible du cortex pré-frontal dorsolatéral comme cible alternative de stimulation.
Central neuropathic pain is a frequent and hard to treat condition. Because of a large amount of drug-refractoriness, neuromodulation techniques have been developed. Among them, the mostly used is motor cortex stimulation, which can be both invasive (epidural motor cortex stimulation (eMCS)) and non-invasive (repetitive magnetic transcranial stimulation (rTMS)). These techniques remain limited by different problems: On one side, rTMS has been mainly studied through unique session practice and its use for pain therapy in a long-term scale remains not well understood. On the other side, eMCS suffers from a lack of predictability: A great proportion of patients present an insufficient relief, making eMCS less and less used. Finally, the motor cortex target is a chance discovery, and some other targets could be intended to improve the results. This work had the increase of knowledge about cortical stimulations as a main goal, especially about their different limitations. This work concentrated on 3 aims: - The study of chronic, repeated sessions of rTMS, used as a long-term tool for pain therapy. - The study of repeated rTMS sessions to predict eMCS.- The development of reliable tool to help to localize others cortical targets.
Advisors/Committee Members: Peyron, Roland (thesis director).
Subjects/Keywords: RTMS; EMCS; Stimulation; Neuromodulation; Douleur neuropathique; Central pain; Neuropathic pain; DLPFC
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APA (6th Edition):
Pommier, B. (2019). Neurostimulations du cortex moteur ou d’ailleurs, invasives ou non, dans la douleur centrale : Cortical neurostimulations, both invasive and non-invasive, to treat central neuropathic pain. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2019LYSES009
Chicago Manual of Style (16th Edition):
Pommier, Benjamin. “Neurostimulations du cortex moteur ou d’ailleurs, invasives ou non, dans la douleur centrale : Cortical neurostimulations, both invasive and non-invasive, to treat central neuropathic pain.” 2019. Doctoral Dissertation, Lyon. Accessed January 28, 2021.
http://www.theses.fr/2019LYSES009.
MLA Handbook (7th Edition):
Pommier, Benjamin. “Neurostimulations du cortex moteur ou d’ailleurs, invasives ou non, dans la douleur centrale : Cortical neurostimulations, both invasive and non-invasive, to treat central neuropathic pain.” 2019. Web. 28 Jan 2021.
Vancouver:
Pommier B. Neurostimulations du cortex moteur ou d’ailleurs, invasives ou non, dans la douleur centrale : Cortical neurostimulations, both invasive and non-invasive, to treat central neuropathic pain. [Internet] [Doctoral dissertation]. Lyon; 2019. [cited 2021 Jan 28].
Available from: http://www.theses.fr/2019LYSES009.
Council of Science Editors:
Pommier B. Neurostimulations du cortex moteur ou d’ailleurs, invasives ou non, dans la douleur centrale : Cortical neurostimulations, both invasive and non-invasive, to treat central neuropathic pain. [Doctoral Dissertation]. Lyon; 2019. Available from: http://www.theses.fr/2019LYSES009
25.
Taliyan, Rajeev.
Possible mechanism of diabetes induced decrease in
antinociceptive effect of analgesics; -.
Degree: pharmacy, 2007, Punjab Technical University
URL: http://shodhganga.inflibnet.ac.in/handle/10603/8938
None
Bibliography p.170-240
Advisors/Committee Members: Sharma, P L.Subjects/Keywords: pharmacy; Pain; Nociceptive Pain; Neuropathic Pain
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APA (6th Edition):
Taliyan, R. (2007). Possible mechanism of diabetes induced decrease in
antinociceptive effect of analgesics; -. (Thesis). Punjab Technical University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/8938
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Taliyan, Rajeev. “Possible mechanism of diabetes induced decrease in
antinociceptive effect of analgesics; -.” 2007. Thesis, Punjab Technical University. Accessed January 28, 2021.
http://shodhganga.inflibnet.ac.in/handle/10603/8938.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Taliyan, Rajeev. “Possible mechanism of diabetes induced decrease in
antinociceptive effect of analgesics; -.” 2007. Web. 28 Jan 2021.
Vancouver:
Taliyan R. Possible mechanism of diabetes induced decrease in
antinociceptive effect of analgesics; -. [Internet] [Thesis]. Punjab Technical University; 2007. [cited 2021 Jan 28].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/8938.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Taliyan R. Possible mechanism of diabetes induced decrease in
antinociceptive effect of analgesics; -. [Thesis]. Punjab Technical University; 2007. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/8938
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Francisco
26.
Storlie, Jessica.
EVIDENCE OF ASSOCIATIONS BETWEEN NEUROTRANSMITTER CANDIDATE GENES AND PERSISTENT ARM PAIN SEVERITY FOLLOWING BREAST CANCER SURGERY.
Degree: Nursing, 2014, University of California – San Francisco
URL: http://www.escholarship.org/uc/item/1tb5z3vd
► Persistent arm pain, a distinct syndrome from persistent breast pain, is a considerable clinical problem following breast cancer surgery. The roles of neurotransmitters and neurotransmitter…
(more)
▼ Persistent arm pain, a distinct syndrome from persistent breast pain, is a considerable clinical problem following breast cancer surgery. The roles of neurotransmitters and neurotransmitter genes have been examined in persistent neuropathic pain; however, genetic associations have not been examined in the setting of breast cancer surgery. In this study, associations between previously identified arm pain classes (i.e., No Arm Pain vs. Mild Arm Pain and No Arm Pain vs. Moderate Arm Pain) and single nucleotide polymorphisms (SNPs) over 30 candidate neurotransmitter genes were evaluated. After multivariate logistic regression analyses for phenotypic characteristics, 4 SNPs and 1 haplotype remained significant between the No Arm Pain and Mild Arm Pain classes: 1 SNP in BDNF (i.e., rs11030102), 1 SNP in COMT (i.e., rs4633), 1 haplotype in HTR2A (i.e., Haplotype B02), 1 SNP for HTR3A (i.e., rs1985242), and 1 SNP in TH (i.e., rs2070762). Between the No Arm Pain and Moderate Arm Pain classes, 9 SNPs remained significant: 1 SNP in BDNF (i.e., rs2049046), 1 SNP in COMT (i.e., rs165656), 2 SNPs in HTR2A (i.e., rs2770298 and rs9534511), 1 SNP in HTR3A (i.e., rs1985242), 1 SNP in NOS2A (i.e., rs2248814), 1 SNP in NPY (i.e., rs16148), 1 SNP in SLC6A1 (i.e., rs2601126), and 1 SNP in TACR1 (i.e., rs4439987). These findings suggest meaningful impact of neurotransmitter genes on the development of persistent arm pain following breast cancer surgery.
Subjects/Keywords: Oncology; Genetics; arm pain; breast cancer; genetics; growth mixture model; neuropathic pain; persistent pain
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APA (6th Edition):
Storlie, J. (2014). EVIDENCE OF ASSOCIATIONS BETWEEN NEUROTRANSMITTER CANDIDATE GENES AND PERSISTENT ARM PAIN SEVERITY FOLLOWING BREAST CANCER SURGERY. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/1tb5z3vd
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Storlie, Jessica. “EVIDENCE OF ASSOCIATIONS BETWEEN NEUROTRANSMITTER CANDIDATE GENES AND PERSISTENT ARM PAIN SEVERITY FOLLOWING BREAST CANCER SURGERY.” 2014. Thesis, University of California – San Francisco. Accessed January 28, 2021.
http://www.escholarship.org/uc/item/1tb5z3vd.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Storlie, Jessica. “EVIDENCE OF ASSOCIATIONS BETWEEN NEUROTRANSMITTER CANDIDATE GENES AND PERSISTENT ARM PAIN SEVERITY FOLLOWING BREAST CANCER SURGERY.” 2014. Web. 28 Jan 2021.
Vancouver:
Storlie J. EVIDENCE OF ASSOCIATIONS BETWEEN NEUROTRANSMITTER CANDIDATE GENES AND PERSISTENT ARM PAIN SEVERITY FOLLOWING BREAST CANCER SURGERY. [Internet] [Thesis]. University of California – San Francisco; 2014. [cited 2021 Jan 28].
Available from: http://www.escholarship.org/uc/item/1tb5z3vd.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Storlie J. EVIDENCE OF ASSOCIATIONS BETWEEN NEUROTRANSMITTER CANDIDATE GENES AND PERSISTENT ARM PAIN SEVERITY FOLLOWING BREAST CANCER SURGERY. [Thesis]. University of California – San Francisco; 2014. Available from: http://www.escholarship.org/uc/item/1tb5z3vd
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Adelaide
27.
Staikopoulos, Vasiliki.
The role of nitroxyl in the development of neuropathic pain.
Degree: 2019, University of Adelaide
URL: http://hdl.handle.net/2440/123423
► Neuropathic pain is a debilitating persistent (chronic) pain condition which affects 2% of the total population, characterised by spontaneous pain (stimulus independent), allodynia (pain generated…
(more)
▼ Neuropathic pain is a debilitating persistent (chronic)
pain condition which affects 2% of the total population, characterised by spontaneous
pain (stimulus independent), allodynia (
pain generated from non-noxious stimuli) and hyperalgesia (heightened sense of
pain to noxious stimuli). Unlike other types of
pain such as nociceptive or inflammatory,
neuropathic pain is maladaptive and therefore neither protects or supports healing or repair. It is defined as “
pain caused by a lesion or disease of the somatosensory nervous system” and can develop following an array of aetiologies such as peripheral or central nerve lesions, diabetes, herpes zoster, HIV and cancer, to name a few. However, resolution of the underlying disease and/or healing of the injury often does not alleviate the associated
neuropathic pain symptoms suggesting that central maladaptive plasticity may occur in people with
neuropathic pain. Compounding this situation, this maladaptive plasticity often renders traditional analgesics used for nociceptive and inflammatory
pain ineffective, thus reducing the treatment options available for
neuropathic pain sufferers. The spinal mechanisms which lead to persistent
pain development have yet to be fully elucidated. It is well understood that adaptations in the reactivity of spinal glial cells (microglia and astrocytes) may also contribute to central neuronal plasticity, by releasing inflammatory mediators such as nitric oxide and other reactive nitrogen species, that enhance excitatory and/or reduce inhibitory neuronal signalling (also referred to as neuro-immune signalling). Previous limitations in methodology have limited our understanding of longitudinal changes in spinal glial during critical developmental stages in persistent
pain pathology. Whether there is a correlation between glial reactivity and
neuropathic pain severity during the development of the disease model, has yet to be established. Therefore, the initial aim of this thesis was to determine if reactivity characteristics of spinal microglia may correlate with peripheral injury severity and subsequent
neuropathic pain symptoms, in mouse models of persistent
pain (Chapter 5). Studies suggest that following peripheral injury, there may be alternative reactive nitrogen species, other than nitric oxide, released by highly reactive glial cells which may facilitate neural plasticity within the spinal cord. The recent development of novel fluorescent tools for measuring reactive nitrogen species, such as nitroxyl, have yet to be used to identify the endogenous presence of this reactive nitrogen species in
neuropathic pain development. Therefore, the second aim of this thesis was to validate the use of a novel fluorescent probe for the detection of endogenous nitroxyl in mouse models of persistent
pain (Chapter 3). The role of nitroxyl in persistent
pain development, has been complicated by recent reports whereby exogenous application of high concentration of this reactive nitrogen species, can act as therapeutic agent for persistent
pain. The…
Advisors/Committee Members: Hutchinson, Mark (advisor), Beckett, Elizabeth (advisor), Adelaide Medical School (school).
Subjects/Keywords: Nitroxyl; pain; neuropathic pain; chronic pain; probes; fluorescent probes; reactive nitrogen species; microglia; glia
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APA ·
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APA (6th Edition):
Staikopoulos, V. (2019). The role of nitroxyl in the development of neuropathic pain. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/123423
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Staikopoulos, Vasiliki. “The role of nitroxyl in the development of neuropathic pain.” 2019. Thesis, University of Adelaide. Accessed January 28, 2021.
http://hdl.handle.net/2440/123423.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Staikopoulos, Vasiliki. “The role of nitroxyl in the development of neuropathic pain.” 2019. Web. 28 Jan 2021.
Vancouver:
Staikopoulos V. The role of nitroxyl in the development of neuropathic pain. [Internet] [Thesis]. University of Adelaide; 2019. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/2440/123423.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Staikopoulos V. The role of nitroxyl in the development of neuropathic pain. [Thesis]. University of Adelaide; 2019. Available from: http://hdl.handle.net/2440/123423
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Punjabi University
28.
Singh, Amteshwar.
Exploring novel pharmacological interventions for
experimental peripheral neuropathy;.
Degree: Pharmaceutical Sciences, 2012, Punjabi University
URL: http://shodhganga.inflibnet.ac.in/handle/10603/8024
None
Summary p. 111-112, References p. 113-155 and List
of Publications p. 156
Advisors/Committee Members: Singh, Nirmal.Subjects/Keywords: Pharmaceutical Sciences; Neuropathic Pain; Neuropathic Pain Management
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APA ·
Chicago ·
MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Singh, A. (2012). Exploring novel pharmacological interventions for
experimental peripheral neuropathy;. (Thesis). Punjabi University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/8024
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Singh, Amteshwar. “Exploring novel pharmacological interventions for
experimental peripheral neuropathy;.” 2012. Thesis, Punjabi University. Accessed January 28, 2021.
http://shodhganga.inflibnet.ac.in/handle/10603/8024.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Singh, Amteshwar. “Exploring novel pharmacological interventions for
experimental peripheral neuropathy;.” 2012. Web. 28 Jan 2021.
Vancouver:
Singh A. Exploring novel pharmacological interventions for
experimental peripheral neuropathy;. [Internet] [Thesis]. Punjabi University; 2012. [cited 2021 Jan 28].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/8024.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Singh A. Exploring novel pharmacological interventions for
experimental peripheral neuropathy;. [Thesis]. Punjabi University; 2012. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/8024
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manitoba
29.
Bokhari, Fozia.
Pilot study of a survey to identify the prevalence and risk factors for chronic neuropathic pain in women following breast cancer surgery.
Degree: Nursing, 2010, University of Manitoba
URL: http://hdl.handle.net/1993/3919
► Breast cancer is the most common cancer among Canadian women. Chronic neuropathic pain post breast surgery (PPBS), also known as chronic post mastectomy/lumpectomy pain syndrome,…
(more)
▼ Breast cancer is the most common cancer among Canadian women. Chronic
neuropathic pain post breast surgery (PPBS), also known as chronic post mastectomy/lumpectomy
pain syndrome, is a poorly understood complication posing a significant clinical challenge with major negative impact on patients' quality of life. This study aims to: 1) provide a preliminary determination of the prevalence rate of women who suffer from PPBS; and 2) explore potential risk factors associated with women developing PPBS. This pilot study used a prospective, longitudinal, quantitative survey design, with a demographic questionnaire and the Brief
Pain Inventory. Seventeen women were recruited at a breast health clinic in Western Canada; 23.5% developed PPBS. Younger age (≤50 years), more invasive surgery, acute post-operative
pain, and less analgesic use at the acute post-operative period, were more commonly found in the women who developed PPBS. Future research is required to confirm the significance of these potential risk factors.
Advisors/Committee Members: McMillan, Diana (Nursing) (supervisor), McClement, Susan (Nursing) Daeninck, Paul (St. Boniface General Hospital) (examiningcommittee).
Subjects/Keywords: breast cancer; neuropathic pain; chronic pain; treatment; breast cancer surgery; postmastectomy pain syndrome; pain syndrome; postlumpectomy pain syndrome
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Export
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APA (6th Edition):
Bokhari, F. (2010). Pilot study of a survey to identify the prevalence and risk factors for chronic neuropathic pain in women following breast cancer surgery. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/3919
Chicago Manual of Style (16th Edition):
Bokhari, Fozia. “Pilot study of a survey to identify the prevalence and risk factors for chronic neuropathic pain in women following breast cancer surgery.” 2010. Masters Thesis, University of Manitoba. Accessed January 28, 2021.
http://hdl.handle.net/1993/3919.
MLA Handbook (7th Edition):
Bokhari, Fozia. “Pilot study of a survey to identify the prevalence and risk factors for chronic neuropathic pain in women following breast cancer surgery.” 2010. Web. 28 Jan 2021.
Vancouver:
Bokhari F. Pilot study of a survey to identify the prevalence and risk factors for chronic neuropathic pain in women following breast cancer surgery. [Internet] [Masters thesis]. University of Manitoba; 2010. [cited 2021 Jan 28].
Available from: http://hdl.handle.net/1993/3919.
Council of Science Editors:
Bokhari F. Pilot study of a survey to identify the prevalence and risk factors for chronic neuropathic pain in women following breast cancer surgery. [Masters Thesis]. University of Manitoba; 2010. Available from: http://hdl.handle.net/1993/3919
NSYSU
30.
Liao , Chang-yi.
The anti-nociceptive effects of a marine-derived peptide in neuropathic rats.
Degree: Master, Marine Biotechnology and Resources, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0826113-170307
► In recent years, marine organism-derived peptides have been identified as new and potential sources for drug development. Recently, we found that the marine organism-derived peptide,…
(more)
▼ In recent years, marine organism-derived peptides have been identified as new and potential sources for drug development. Recently, we found that the marine organism-derived peptide, PCD-1 was biologically active, and previous studies have indicated that it have anti-inflammatory properties. The neuroinflammatory processes are known to play a critical role in the development and maintenance of
neuropathic pain, for which no effective drugs are currently available. In the present study, we investigated the anti-analgesic and anti-neuroinflammatory effects of the PCD-1 on chronic constriction injury-induced neuropathy in rats. We found that intrathecal injection of PCD-1 produced a significant and dose-dependent inhibition of thermal hyperalgesia, mechanical allodynia, weight bearing, and cold allodynia in
neuropathic rats after CCI surgery. Moreover, it also attenuated CCI-induced spinal neuroinflammation. On the basis of these experimental results, we suggest that PCD-1 could be used as a potential therapeutic agent for
neuropathic pain.
Advisors/Committee Members: Zhi-Hong Wen (committee member), San-Nan Yang (chair), Jyh-Yih Chen (chair).
Subjects/Keywords: neuropathic pain; microglia; chronic constrictive injury; marine-derived peptide
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APA ·
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APA (6th Edition):
Liao , C. (2013). The anti-nociceptive effects of a marine-derived peptide in neuropathic rats. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0826113-170307
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liao , Chang-yi. “The anti-nociceptive effects of a marine-derived peptide in neuropathic rats.” 2013. Thesis, NSYSU. Accessed January 28, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0826113-170307.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liao , Chang-yi. “The anti-nociceptive effects of a marine-derived peptide in neuropathic rats.” 2013. Web. 28 Jan 2021.
Vancouver:
Liao C. The anti-nociceptive effects of a marine-derived peptide in neuropathic rats. [Internet] [Thesis]. NSYSU; 2013. [cited 2021 Jan 28].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0826113-170307.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liao C. The anti-nociceptive effects of a marine-derived peptide in neuropathic rats. [Thesis]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0826113-170307
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
◁ [1] [2] [3] [4] [5] [6] [7] [8] [9] ▶
. 
Open Access Theses and Dissertations