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You searched for +publisher:"Indian Institute of Science" +contributor:("Sikdar, S K"). Showing records 1 – 3 of 3 total matches.

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Indian Institute of Science

1. Padmashri, R. Intracellular Calcium Dynamics In Dendrites Of Hippocampal Neurons Rendered Epileptic And In Processes Of Astrocytes Following Glutamate Pretreatment.

Degree: 2006, Indian Institute of Science

The fundamental attribute of neurons is their cellular electrical excitability, which is based on the expression of a plethora of ligand- and voltage-gated membrane channels that give rise to prominent membrane currents and membrane potential variations that represent the biophysical substrate underlying the transfer and integration of information at the cellular level. Dendrites have both an electrical and a biochemical character, which are closely linked. In contrast, glial cells are non-electrically excitable but nevertheless display a form of excitability that is based on variations of the Ca2+ concentration in the cytosol rather than electrical changes in the membrane. Cytoplasmic Ca2+ serves as an intracellular signal that is responsible for controlling a multitude of cellular processes. The key to this pleiotropic role is the complex spatiotemporal organization of the [Ca2+]i rise evoked by extracellular agonists, which allows selected effectors to be recruited and specific actions to be initiated. Ca2+ handling in the cell is maintained by operation of multiple mechanisms of Ca2+ influx, internal release, diffusion, buffering and extrusion. Ca2+ tends to be a rather parochial operator with a small radius of action from its point of entry at the cytoplasm resulting in the concept of microdomains. Dendritic Ca2+ signaling have been shown to be highly compartmentalized and astrocytic processes have been reported to be constituted by hundreds of microdomains that represent the elementary units of the astrocyte Ca2+ signal, from where it can eventually propagate to other regions of the cell. The astrocyte Ca2+ elevation may thus act as intra and intercellular signal that can propagate within and between astrocytes, signaling to different regions of the cell and to different cells. The spatio-temporal features of neuron-to-astrocyte communication, results from diverse neurotransmitters and signaling pathways that converge and cooperate to shape the Ca2+ signal in astrocytes. Alterations in Ca2+ homeostasis have been shown to be associated with major pathological conditions of the brain such as epilepsy, ischemia and neurodegenerative diseases. Although there are evidences of Ca2+ rise in hippocampal neurons in in vitro models of epilepsy (Pal et al., 1999; Limbrick et al., 2001), there is no information on the Ca2+ regulatory mechanisms operating in discrete compartments of the epileptic neuron following Ca2+ influx through voltage gated calcium channels (VGCCs). In the first part of the work, the spatial and temporal profiles of depolarization induced changes in the intracellular Ca2+ concentration in the dendrites of cultured autaptic hippocampal pyramidal neurons rendered epileptic experimentally have been addressed. Our in vitro epilepsy model consisted of hippocampal neurons in autaptic culture that were grown in the presence of kynurenate and high Mg2+, and subsequently washing the preparation free of the blockers. To understand the differences in Ca2+ handling mechanisms in different compartments of a… Advisors/Committee Members: Sikdar, S K.

Subjects/Keywords: Calcium - Biochemistry; Calcium Ion Signaling; Voltage-gated Ion Channels; Hippocampal Neurons; Astrocytes; Calcium Dynamics; Glutamate; Dendrites; Status Epilepticus (SE); Astrocyte Pairs; Biochemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Padmashri, R. (2006). Intracellular Calcium Dynamics In Dendrites Of Hippocampal Neurons Rendered Epileptic And In Processes Of Astrocytes Following Glutamate Pretreatment. (Thesis). Indian Institute of Science. Retrieved from http://hdl.handle.net/2005/450

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):

Padmashri, R. “Intracellular Calcium Dynamics In Dendrites Of Hippocampal Neurons Rendered Epileptic And In Processes Of Astrocytes Following Glutamate Pretreatment.” 2006. Thesis, Indian Institute of Science. Accessed September 15, 2019. http://hdl.handle.net/2005/450.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Padmashri, R. “Intracellular Calcium Dynamics In Dendrites Of Hippocampal Neurons Rendered Epileptic And In Processes Of Astrocytes Following Glutamate Pretreatment.” 2006. Web. 15 Sep 2019.

Vancouver:

Padmashri R. Intracellular Calcium Dynamics In Dendrites Of Hippocampal Neurons Rendered Epileptic And In Processes Of Astrocytes Following Glutamate Pretreatment. [Internet] [Thesis]. Indian Institute of Science; 2006. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/2005/450.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Padmashri R. Intracellular Calcium Dynamics In Dendrites Of Hippocampal Neurons Rendered Epileptic And In Processes Of Astrocytes Following Glutamate Pretreatment. [Thesis]. Indian Institute of Science; 2006. Available from: http://hdl.handle.net/2005/450

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Indian Institute of Science

2. Harinath, S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.

Degree: 2005, Indian Institute of Science

Background potassium currents play an important role in the regulation of the resting membrane potential and excitability of mammalian neurons. Recently cloned two- pore domain potassium channels (K2p) are believed to underlie these currents. The roles of K2P channels in general anesthesia and neuroprotection have been proposed recently. In view of this, we investigated the ability of trichloroethanol (an active metabolite of the non-volatile general anesthetic cldoral hydrate, widely used as a pediatric sedative) to modulate the activity of human TREK-1 and TRAAK channels. We found that trichloroethanol potently activates both hTREK-1 and hTRAAK channels at pharmacologically relevant concentrations. The parent compound chloral hydrate was also found to augtnent the activity of both the channels reversibly. Studies with carboxy- terminal deletion mutants (hTREK-1A89, hTREK-1 A100 and hTREK-1 A1 19), suggested that C-terminal tail is not essential for the activation of TREK-1 by trichloroethanol. Our findings identify TREK-1 and TRCL4K channels as molecular targets for trichloroethanol and we propose that activation of both these channels might contribute to the CNS depressant effects of chloral hydrate. Another channel TASK-2, which is essentially absent in the human brain was also found to be potently activated by both trichloroethanol and chloral hydrate. In another series of experiments, we studied the effects of methyl xanthines caffeine and theophylline on hTREK-1 channels. Caffeine and theophylline are used for therapeutic purposes and frequently cause life-threatening convulsive seizures due to systemic toxicity. The mechanisms for the epileptogenicity of caffeine and theophylline are not clear. Recent experiments using knockout mice provided direct evidence for a role for TREK-1 in the control of epileptogenesis. We hypothesized that the epileptogenicity of caffeine and theophylline may be related to the inhibition of TREK-1 channels. We investigated this possibility and observed massive inhibition of TREK-1 channels at toxicologically relevant concentrations. Experiments with the mutant TREK-1 channel (S348A mutant) suggested the involvement of cANP/PKA pathway in the inhibition of TREK-1 channels by caffeine and theophylline. We suggest that inhibition of TREK-1 channels may contribute to the convulsive seizures induced by toxic levels of caffeine and theophylline. Local anesthetics exhibit their clinical effects not only by binding to voltage-gated sodium channels, but also by interacting with other ion channels such as potassium channels. Because of the physiological significance of TREK-1 channels and their abundant expression in peripheral sensory neurons, we investigated the effects of lidocaine to see whether its interaction with 'REK-1 channels contribute to the conduction blockade. Lidocaine caused dose-dependent inhibition of TREK-1channels and the inhibition was voltage-independent. Cytoplasmic C-terminal tail is critically required for lidocaine action. Inhibition of TREK-1 channels is… Advisors/Committee Members: Sikdar, S K.

Subjects/Keywords: K Channels - Physiology; K Channels - Pharmacology; Cell Patch-Clamp Analysis; Ion Channels; Two-Pore Domain Potassium Channels; K+ Channels; TREK-1 Channels; TRAAK Channels; Caffeine; Theophylline; K2P Channels; Molecular Biology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Harinath, S. (2005). Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. (Thesis). Indian Institute of Science. Retrieved from http://hdl.handle.net/2005/1501

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):

Harinath, S. “Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.” 2005. Thesis, Indian Institute of Science. Accessed September 15, 2019. http://hdl.handle.net/2005/1501.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Harinath, S. “Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.” 2005. Web. 15 Sep 2019.

Vancouver:

Harinath S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. [Internet] [Thesis]. Indian Institute of Science; 2005. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/2005/1501.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Harinath S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. [Thesis]. Indian Institute of Science; 2005. Available from: http://hdl.handle.net/2005/1501

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Indian Institute of Science

3. Harinath, S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.

Degree: 2005, Indian Institute of Science

Background potassium currents play an important role in the regulation of the resting membrane potential and excitability of mammalian neurons. Recently cloned two- pore domain potassium channels (K2p) are believed to underlie these currents. The roles of K2P channels in general anesthesia and neuroprotection have been proposed recently. In view of this, we investigated the ability of trichloroethanol (an active metabolite of the non-volatile general anesthetic cldoral hydrate, widely used as a pediatric sedative) to modulate the activity of human TREK-1 and TRAAK channels. We found that trichloroethanol potently activates both hTREK-1 and hTRAAK channels at pharmacologically relevant concentrations. The parent compound chloral hydrate was also found to augtnent the activity of both the channels reversibly. Studies with carboxy- terminal deletion mutants (hTREK-1A89, hTREK-1 A100 and hTREK-1 A1 19), suggested that C-terminal tail is not essential for the activation of TREK-1 by trichloroethanol. Our findings identify TREK-1 and TRCL4K channels as molecular targets for trichloroethanol and we propose that activation of both these channels might contribute to the CNS depressant effects of chloral hydrate. Another channel TASK-2, which is essentially absent in the human brain was also found to be potently activated by both trichloroethanol and chloral hydrate. In another series of experiments, we studied the effects of methyl xanthines caffeine and theophylline on hTREK-1 channels. Caffeine and theophylline are used for therapeutic purposes and frequently cause life-threatening convulsive seizures due to systemic toxicity. The mechanisms for the epileptogenicity of caffeine and theophylline are not clear. Recent experiments using knockout mice provided direct evidence for a role for TREK-1 in the control of epileptogenesis. We hypothesized that the epileptogenicity of caffeine and theophylline may be related to the inhibition of TREK-1 channels. We investigated this possibility and observed massive inhibition of TREK-1 channels at toxicologically relevant concentrations. Experiments with the mutant TREK-1 channel (S348A mutant) suggested the involvement of cANP/PKA pathway in the inhibition of TREK-1 channels by caffeine and theophylline. We suggest that inhibition of TREK-1 channels may contribute to the convulsive seizures induced by toxic levels of caffeine and theophylline. Local anesthetics exhibit their clinical effects not only by binding to voltage-gated sodium channels, but also by interacting with other ion channels such as potassium channels. Because of the physiological significance of TREK-1 channels and their abundant expression in peripheral sensory neurons, we investigated the effects of lidocaine to see whether its interaction with 'REK-1 channels contribute to the conduction blockade. Lidocaine caused dose-dependent inhibition of TREK-1channels and the inhibition was voltage-independent. Cytoplasmic C-terminal tail is critically required for lidocaine action. Inhibition of TREK-1 channels is… Advisors/Committee Members: Sikdar, S K.

Subjects/Keywords: K Channels - Physiology; K Channels - Pharmacology; Cell Patch-Clamp Analysis; Ion Channels; Two-Pore Domain Potassium Channels; K+ Channels; TREK-1 Channels; TRAAK Channels; Caffeine; Theophylline; K2P Channels; Molecular Biology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Harinath, S. (2005). Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. (Thesis). Indian Institute of Science. Retrieved from http://etd.iisc.ernet.in/handle/2005/1501 ; http://etd.ncsi.iisc.ernet.in/abstracts/1921/G19592-Abs.pdf

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):

Harinath, S. “Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.” 2005. Thesis, Indian Institute of Science. Accessed September 15, 2019. http://etd.iisc.ernet.in/handle/2005/1501 ; http://etd.ncsi.iisc.ernet.in/abstracts/1921/G19592-Abs.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Harinath, S. “Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis.” 2005. Web. 15 Sep 2019.

Vancouver:

Harinath S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. [Internet] [Thesis]. Indian Institute of Science; 2005. [cited 2019 Sep 15]. Available from: http://etd.iisc.ernet.in/handle/2005/1501 ; http://etd.ncsi.iisc.ernet.in/abstracts/1921/G19592-Abs.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Harinath S. Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis. [Thesis]. Indian Institute of Science; 2005. Available from: http://etd.iisc.ernet.in/handle/2005/1501 ; http://etd.ncsi.iisc.ernet.in/abstracts/1921/G19592-Abs.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.