Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors

Serotonin receptors are targets of drug therapies for a variety of neuropsychiatric and neurodegenerative disorders. Cocaine inhibits the re-uptake of serotonin (5-HT), dopamine, and noradrenaline, whereas caffeine blocks adenosine receptors and opens ryanodine receptors in the endoplasmic reticulum...

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Autores principales: Goitia, Belen, Weisstaub, Noelia V.
Publicado: 2016
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00223042_v136_n3_p526_Goitia
http://hdl.handle.net/20.500.12110/paper_00223042_v136_n3_p526_Goitia
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id paper:paper_00223042_v136_n3_p526_Goitia
record_format dspace
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic caffeine
cocaine
GABA
serotonin
thalamic reticular nucleus
1 (2 methoxyphenyl) 4 (4 phthalimidobutyl)piperazine
adenosine
caffeine
cocaine
serotonin
serotonin 1A receptor
serotonin 2A receptor
serotonin receptor
4 aminobutyric acid
cadmium chloride
caffeine
cocaine
dopamine uptake inhibitor
inositol 1,4,5 trisphosphate
phosphodiesterase inhibitor
phospholipase C
serotonin
serotonin 2A receptor
serotonin receptor affecting agent
4 aminobutyric acid release
animal experiment
animal tissue
Article
concentration (parameters)
controlled study
excitatory postsynaptic potential
GABAergic transmission
inhibition kinetics
male
mouse
neuromodulation
nonhuman
pharmacological blocking
priority journal
serotoninergic system
thalamus reticular nucleus
thalamus ventral nucleus
whole cell patch clamp
action potential
animal
dose response
drug effects
genetics
in vitro study
knockout mouse
metabolism
patch clamp technique
thalamus nucleus
Action Potentials
Animals
Cadmium Chloride
Caffeine
Cocaine
Dopamine Uptake Inhibitors
Dose-Response Relationship, Drug
gamma-Aminobutyric Acid
In Vitro Techniques
Inositol 1,4,5-Trisphosphate
Male
Mice
Mice, Knockout
Patch-Clamp Techniques
Phosphodiesterase Inhibitors
Receptor, Serotonin, 5-HT2A
Serotonin
Serotonin Agents
Thalamic Nuclei
Type C Phospholipases
spellingShingle caffeine
cocaine
GABA
serotonin
thalamic reticular nucleus
1 (2 methoxyphenyl) 4 (4 phthalimidobutyl)piperazine
adenosine
caffeine
cocaine
serotonin
serotonin 1A receptor
serotonin 2A receptor
serotonin receptor
4 aminobutyric acid
cadmium chloride
caffeine
cocaine
dopamine uptake inhibitor
inositol 1,4,5 trisphosphate
phosphodiesterase inhibitor
phospholipase C
serotonin
serotonin 2A receptor
serotonin receptor affecting agent
4 aminobutyric acid release
animal experiment
animal tissue
Article
concentration (parameters)
controlled study
excitatory postsynaptic potential
GABAergic transmission
inhibition kinetics
male
mouse
neuromodulation
nonhuman
pharmacological blocking
priority journal
serotoninergic system
thalamus reticular nucleus
thalamus ventral nucleus
whole cell patch clamp
action potential
animal
dose response
drug effects
genetics
in vitro study
knockout mouse
metabolism
patch clamp technique
thalamus nucleus
Action Potentials
Animals
Cadmium Chloride
Caffeine
Cocaine
Dopamine Uptake Inhibitors
Dose-Response Relationship, Drug
gamma-Aminobutyric Acid
In Vitro Techniques
Inositol 1,4,5-Trisphosphate
Male
Mice
Mice, Knockout
Patch-Clamp Techniques
Phosphodiesterase Inhibitors
Receptor, Serotonin, 5-HT2A
Serotonin
Serotonin Agents
Thalamic Nuclei
Type C Phospholipases
Goitia, Belen
Weisstaub, Noelia V.
Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
topic_facet caffeine
cocaine
GABA
serotonin
thalamic reticular nucleus
1 (2 methoxyphenyl) 4 (4 phthalimidobutyl)piperazine
adenosine
caffeine
cocaine
serotonin
serotonin 1A receptor
serotonin 2A receptor
serotonin receptor
4 aminobutyric acid
cadmium chloride
caffeine
cocaine
dopamine uptake inhibitor
inositol 1,4,5 trisphosphate
phosphodiesterase inhibitor
phospholipase C
serotonin
serotonin 2A receptor
serotonin receptor affecting agent
4 aminobutyric acid release
animal experiment
animal tissue
Article
concentration (parameters)
controlled study
excitatory postsynaptic potential
GABAergic transmission
inhibition kinetics
male
mouse
neuromodulation
nonhuman
pharmacological blocking
priority journal
serotoninergic system
thalamus reticular nucleus
thalamus ventral nucleus
whole cell patch clamp
action potential
animal
dose response
drug effects
genetics
in vitro study
knockout mouse
metabolism
patch clamp technique
thalamus nucleus
Action Potentials
Animals
Cadmium Chloride
Caffeine
Cocaine
Dopamine Uptake Inhibitors
Dose-Response Relationship, Drug
gamma-Aminobutyric Acid
In Vitro Techniques
Inositol 1,4,5-Trisphosphate
Male
Mice
Mice, Knockout
Patch-Clamp Techniques
Phosphodiesterase Inhibitors
Receptor, Serotonin, 5-HT2A
Serotonin
Serotonin Agents
Thalamic Nuclei
Type C Phospholipases
description Serotonin receptors are targets of drug therapies for a variety of neuropsychiatric and neurodegenerative disorders. Cocaine inhibits the re-uptake of serotonin (5-HT), dopamine, and noradrenaline, whereas caffeine blocks adenosine receptors and opens ryanodine receptors in the endoplasmic reticulum. We studied how 5-HT and adenosine affected spontaneous GABAergic transmission from thalamic reticular nucleus. We combined whole-cell patch clamp recordings of miniature inhibitory post-synaptic currents (mIPSCs) in ventrobasal thalamic neurons during local (puff) application of 5-HT in wild type (WT) or knockout mice lacking 5-HT 2A receptors (5-HT 2A -/-). Inhibition of mIPSCs frequency by low (10 μM) and high (100 μM) 5-HT concentrations was observed in ventrobasal neurons from 5-HT 2A -/- mice. In WT mice, only 100 μM 5-HT significantly reduced mIPSCs frequency. In 5-HT 2A -/- mice, NAN-190, a specific 5-HT 1A antagonist, prevented the 100 μM 5-HT inhibition while blocking H-currents that prolonged inhibition during post-puff periods. The inhibitory effects of 100 μM 5-HT were enhanced in cocaine binge-treated 5-HT 2A -/- mice. Caffeine binge treatment did not affect 5-HT-mediated inhibition. Our findings suggest that both 5-HT 1A and 5-HT 2A receptors are present in pre-synaptic thalamic reticular nucleus terminals. Serotonergic-mediated inhibition of GABA release could underlie aberrant thalamocortical physiology described after repetitive consumption of cocaine. Our findings suggest that both 5-HT 1A , 5-HT 2A and A1 receptors are present in pre-synaptic TRN terminals. 5-HT 1A and A1 receptors would down-regulate adenylate cyclase, whereas 5-HT 1A would also increase the probability of the opening of G-protein-activated inwardly rectifying K + channels (GIRK). Sustained opening of GIRK channels would hyperpolarize pre-synaptic terminals activating H-currents, resulting in less GABA release. 5-HT 2A -would activate PLC and IP 3 , increasing intracellular [Ca 2+ ] and thus facilitating GABA release. Our findings suggest that both 5-HT 1A , 5-HT 2A and A1 receptors are present in pre-synaptic TRN terminals. 5-HT 1A and A1 receptors would down-regulate adenylate cyclase, whereas 5-HT 1A would also increase the probability of the opening of G-protein-activated inwardly rectifying K + channels (GIRK). Sustained opening of GIRK channels would hyperpolarize pre-synaptic terminals activating H-currents, resulting in less GABA release. 5-HT 2A -would activate PLC and IP 3 , increasing intracellular [Ca 2+ ] and thus facilitating GABA release. © 2015 International Society for Neurochemistry.
author Goitia, Belen
Weisstaub, Noelia V.
author_facet Goitia, Belen
Weisstaub, Noelia V.
author_sort Goitia, Belen
title Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
title_short Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
title_full Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
title_fullStr Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
title_full_unstemmed Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
title_sort modulation of gaba release from the thalamic reticular nucleus by cocaine and caffeine: role of serotonin receptors
publishDate 2016
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00223042_v136_n3_p526_Goitia
http://hdl.handle.net/20.500.12110/paper_00223042_v136_n3_p526_Goitia
work_keys_str_mv AT goitiabelen modulationofgabareleasefromthethalamicreticularnucleusbycocaineandcaffeineroleofserotoninreceptors
AT weisstaubnoeliav modulationofgabareleasefromthethalamicreticularnucleusbycocaineandcaffeineroleofserotoninreceptors
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spelling paper:paper_00223042_v136_n3_p526_Goitia2023-06-08T14:49:06Z Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors Goitia, Belen Weisstaub, Noelia V. caffeine cocaine GABA serotonin thalamic reticular nucleus 1 (2 methoxyphenyl) 4 (4 phthalimidobutyl)piperazine adenosine caffeine cocaine serotonin serotonin 1A receptor serotonin 2A receptor serotonin receptor 4 aminobutyric acid cadmium chloride caffeine cocaine dopamine uptake inhibitor inositol 1,4,5 trisphosphate phosphodiesterase inhibitor phospholipase C serotonin serotonin 2A receptor serotonin receptor affecting agent 4 aminobutyric acid release animal experiment animal tissue Article concentration (parameters) controlled study excitatory postsynaptic potential GABAergic transmission inhibition kinetics male mouse neuromodulation nonhuman pharmacological blocking priority journal serotoninergic system thalamus reticular nucleus thalamus ventral nucleus whole cell patch clamp action potential animal dose response drug effects genetics in vitro study knockout mouse metabolism patch clamp technique thalamus nucleus Action Potentials Animals Cadmium Chloride Caffeine Cocaine Dopamine Uptake Inhibitors Dose-Response Relationship, Drug gamma-Aminobutyric Acid In Vitro Techniques Inositol 1,4,5-Trisphosphate Male Mice Mice, Knockout Patch-Clamp Techniques Phosphodiesterase Inhibitors Receptor, Serotonin, 5-HT2A Serotonin Serotonin Agents Thalamic Nuclei Type C Phospholipases Serotonin receptors are targets of drug therapies for a variety of neuropsychiatric and neurodegenerative disorders. Cocaine inhibits the re-uptake of serotonin (5-HT), dopamine, and noradrenaline, whereas caffeine blocks adenosine receptors and opens ryanodine receptors in the endoplasmic reticulum. We studied how 5-HT and adenosine affected spontaneous GABAergic transmission from thalamic reticular nucleus. We combined whole-cell patch clamp recordings of miniature inhibitory post-synaptic currents (mIPSCs) in ventrobasal thalamic neurons during local (puff) application of 5-HT in wild type (WT) or knockout mice lacking 5-HT 2A receptors (5-HT 2A -/-). Inhibition of mIPSCs frequency by low (10 μM) and high (100 μM) 5-HT concentrations was observed in ventrobasal neurons from 5-HT 2A -/- mice. In WT mice, only 100 μM 5-HT significantly reduced mIPSCs frequency. In 5-HT 2A -/- mice, NAN-190, a specific 5-HT 1A antagonist, prevented the 100 μM 5-HT inhibition while blocking H-currents that prolonged inhibition during post-puff periods. The inhibitory effects of 100 μM 5-HT were enhanced in cocaine binge-treated 5-HT 2A -/- mice. Caffeine binge treatment did not affect 5-HT-mediated inhibition. Our findings suggest that both 5-HT 1A and 5-HT 2A receptors are present in pre-synaptic thalamic reticular nucleus terminals. Serotonergic-mediated inhibition of GABA release could underlie aberrant thalamocortical physiology described after repetitive consumption of cocaine. Our findings suggest that both 5-HT 1A , 5-HT 2A and A1 receptors are present in pre-synaptic TRN terminals. 5-HT 1A and A1 receptors would down-regulate adenylate cyclase, whereas 5-HT 1A would also increase the probability of the opening of G-protein-activated inwardly rectifying K + channels (GIRK). Sustained opening of GIRK channels would hyperpolarize pre-synaptic terminals activating H-currents, resulting in less GABA release. 5-HT 2A -would activate PLC and IP 3 , increasing intracellular [Ca 2+ ] and thus facilitating GABA release. Our findings suggest that both 5-HT 1A , 5-HT 2A and A1 receptors are present in pre-synaptic TRN terminals. 5-HT 1A and A1 receptors would down-regulate adenylate cyclase, whereas 5-HT 1A would also increase the probability of the opening of G-protein-activated inwardly rectifying K + channels (GIRK). Sustained opening of GIRK channels would hyperpolarize pre-synaptic terminals activating H-currents, resulting in less GABA release. 5-HT 2A -would activate PLC and IP 3 , increasing intracellular [Ca 2+ ] and thus facilitating GABA release. © 2015 International Society for Neurochemistry. Fil:Goitia, B. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Weisstaub, N.V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2016 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00223042_v136_n3_p526_Goitia http://hdl.handle.net/20.500.12110/paper_00223042_v136_n3_p526_Goitia