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A model of CA2+ channel opening in response to action potential widening
Title
A model of CA2+ channel opening in response to action potential widening.
Creator
Tranquil, Elizabeth, Rowan, Matthew, Christie, Jason
Date Issued
2013-04-05
PURL
http://purl.flvc.org/fcla/dt/3361215
Subject Headings
Calcium channels, Action Potentials
Format
Document (PDF)
SELECTIVE MODULATION OF SMALL CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNELS IN C57BL/6J MICE RESCUES MEMORY AND ATTENTION DISORDERS IN KETAMINE-INDUCED PSYCHOSIS: A NEW THERAPEUTIC APPROACH
Title
SELECTIVE MODULATION OF SMALL CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNELS IN C57BL/6J MICE RESCUES MEMORY AND ATTENTION DISORDERS IN KETAMINE-INDUCED PSYCHOSIS: A NEW THERAPEUTIC APPROACH.
Creator
Rice, Claire A., Stackman, Jr. Robert W., Florida Atlantic University, Department of Psychology, Charles E. Schmidt College of Science
Abstract/Description
Small conductance Ca2+-activated K+ (SK) channels are expressed throughout brain regions important for long-term memory. They constrain the intrinsic excitability of neurons by enhancing afterhyperpolarization, shape glutamatergic synaptic potentials and limit induction of NMDA receptor-dependent synaptic plasticity. Behaviorally, SK channels modulate learning and memory encoding. It is hypothesized that SK channels influence cognitive symptoms of psychosis including executive functioning,...
Show moreSmall conductance Ca2+-activated K+ (SK) channels are expressed throughout brain regions important for long-term memory. They constrain the intrinsic excitability of neurons by enhancing afterhyperpolarization, shape glutamatergic synaptic potentials and limit induction of NMDA receptor-dependent synaptic plasticity. Behaviorally, SK channels modulate learning and memory encoding. It is hypothesized that SK channels influence cognitive symptoms of psychosis including executive functioning, working memory, and selective attention. Theories of psychosis currently posit that symptoms of psychosis are a result of dopaminergic hyperfunction, and glutamatergic dysregulation which can be induced following administration of the NMDA receptor antagonist, ketamine. Initial experiments confirmed that sub-chronic treatment with KET produced significant impairment of object recognition memory, trace fear memory, and latent inhibition compared to SAL mice. A comparison of ketamine dosing regimens revealed the necessity for sub-chronic/chronic dosing on a consistent schedule with a wash out period, to obtain long-lasting attention and memory impairment. These experiments revealed for the first time that sub-chronic KET treatment elicited a new phenotype in male C57BL/6J mice: audible vocalizations. KET mice emitted audible vocalizations within 10 min of receiving KET injections, and vocalizations were detected up to 30 min after injection. Experiments conducted to determine the efficacy of SK channel agonists and antagonists on SK channels to modulate attention and memory in the ketamineinduced model of psychosis in C57BL/6J mice demonstrated for the first time that the SK2 channel activator, CyPPA, significantly reduced memory impairment and decreased the attention deficit of KET mice. A new method of analysis for trace fear conditioning freezing responses permitted a more accurate measurement of the ability of mice to discriminate the predicted delivery of shock during trace versus CS intervals. The application of the novel analytical method further demonstrated that KET mice failed to accurately discriminate these intervals, due to their impaired attention and acquisition of the trace conditioned response. This study examined the efficacy of SK channel drugs to rescue cognitive impairments in a pharmacological mouse model of schizophrenia. The results indicate that SK2 subunit activators and blockers, may provide a new therapeutic treatment for memory impairment and attention deficits seen in schizophrenic disorders.
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Date Issued
2020
PURL
http://purl.flvc.org/fau/fd/FA00013624
Subject Headings
Calcium-activated potassium channels, Calcium-dependent potassium channels, Mice, Ketamine, Psychoses
Format
Document (PDF)
In vivo administration of a subtype selective activator of small conductance Ca2+ - activated K+ channels influences hippocampal-dependent spatial memory
Title
In vivo administration of a subtype selective activator of small conductance Ca2+ - activated K+ channels influences hippocampal-dependent spatial memory.
Creator
Beck, Robert, Kuchera, Claire Rice, Munchow, Alcira H., Stackman, Robert W., Graduate College
Date Issued
2013-04-12
PURL
http://purl.flvc.org/fcla/dt/3361271
Subject Headings
Calcium-dependent potassium channels, Hippocampus (Brain), Mice, Memory
Format
Document (PDF)
Hurst analysis applied to the study of single calcium-activated potassium channel kinetics
Title
Hurst analysis applied to the study of single calcium-activated potassium channel kinetics.
Creator
Liebovitch, Larry S., Figueiroa, Josed N., Nogueira, Romildo A., Varanda, Wamberto A.
Date Issued
2000-10-07
PURL
http://purl.flvc.org/FAU/165249
Subject Headings
Ion channels-Mathematical models, Memory, Chemical kinetics, Calcium channels, Fractals, Markov processes, Leydig cells, Molecular biology--Statistical methods
Format
Document (PDF)
Protecting Synaptic Function From Acute Oxidative Stress: A Novel Role For Big K+ (BK) Channels And Resveratrol-Like Compounds
Title
Protecting Synaptic Function From Acute Oxidative Stress: A Novel Role For Big K+ (BK) Channels And Resveratrol-Like Compounds.
Creator
Bollinger, Wesley L., Dawson-Scully, Ken, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description
Oxidative stress causes neural damage and inhibits essential cellular processes, such as synaptic transmission. Despite this knowledge, currently available pharmaceutical agents cannot effectively protect neural cells from acute oxidative stress elicited by strokes, heart attacks, and traumatic brain injuries in a real life clinical setting. Our lab has developed an electrophysiology protocol to identify novel drugs that protect an essential cellular process (neurotransmission) from acute...
Show moreOxidative stress causes neural damage and inhibits essential cellular processes, such as synaptic transmission. Despite this knowledge, currently available pharmaceutical agents cannot effectively protect neural cells from acute oxidative stress elicited by strokes, heart attacks, and traumatic brain injuries in a real life clinical setting. Our lab has developed an electrophysiology protocol to identify novel drugs that protect an essential cellular process (neurotransmission) from acute oxidative stress-induced damage. Through this doctoral dissertation, we have identified three new drugs, including a Big K+ (BK) K+ channel blocker (iberiotoxin), resveratrol, and a custom made resveratrol-like compound (fly2) that protect synaptic function from oxidative stress-induced insults. Further developing these drugs as neuroprotective agents may prove transformative in protecting the human brain from acute oxidative stress elicited by strokes, heart attacks, and traumatic brain injuries. Inhibiting the protein kinase G (PKG) pathway protects neurotransmission from acute oxidative stress. This dissertation has expanded upon these findings by determining that the PKG pathway and BK K+ channels function through independent biochemical pathways to protect neurotransmission from acute oxidative stress. Taken together, this dissertation has identified two classes of compounds that protect neurotransmission from acute oxidative stress, including resveratrol-like compounds (resveratrol, fly2) and a BK K+ channel inhibitor (iberiotoxin). Further developing these drugs in clinical trials may finally lead to the development of an effective neuroprotective agent.
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Date Issued
2018
PURL
http://purl.flvc.org/fau/fd/FA00013054
Subject Headings
Neural transmission., Oxidative stress., Large-Conductance Calcium-Activated Potassium Channels., Neuroprotective Agents.
Format
Document (PDF)
Reciprocal regulation between taurine and glutamate response via Ca2+ - dependent pathways in retinal third-order neurons
Title
Reciprocal regulation between taurine and glutamate response via Ca2+ - dependent pathways in retinal third-order neurons.
Creator
Bulley, Simon, Shen, Wen
Date Issued
2010-08-24
PURL
http://purl.flvc.org/fcla/dt/3327274
Subject Headings
Amacrine Cells*/cytology, Amacrine Cells*/drug effects, Amacrine Cells*/metabolism, Ambystoma, Calcium/metabolism, Calcium Channels/metabolism, Cells, Cultured, Enzyme Inhibitors/metabolism, Excitatory Amino Acid Agonists/pharmacology, GABA Antagonists/pharmacology, Glutamic Acid/metabolism, Glycine Agents/pharmacology, Kainic Acid/pharmacology, Membrane Glycoproteins, Membrane Potentials, Neurotransmitter Agents, Retinal Ganglion Cells, Signal Transduction, Synaptic Transmission
Format
Document (PDF)