Cocaine acute "binge" administration results in altered thalamocortical interactions in mice

Background: Abnormalities in both thalamic and cortical areas have been reported in human cocaine addicts with noninvasive functional magnetic resonance imaging. Given the substantial involvement of the thalamocortical system in sensory processing and perception, we defined electrophysiology-based p...

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Publicado:	2009
Materias:	Cocaine GABA-A receptors Mice T-type calcium channels Thalamocortical dysrhythmia 2 amino 5 phosphonovaleric acid 4 aminobutyric acid A receptor 6 cyano 7 nitro 2,3 quinoxalinedione AMPA receptor antagonist calcium channel T type cesium cocaine kainic acid receptor antagonist n methyl dextro aspartic acid receptor blocking agent picrotoxin potassium ion tetrodotoxin animal cell animal experiment animal model animal tissue article brain function brain slice cocaine dependence drug abuse electroencephalography in vitro study in vivo study mouse neurotransmitter release nonhuman patch clamp priority journal thalamocortical tract voltage clamp animal brain cortex C57BL mouse cell membrane potential drug antagonism drug effect drug interaction drug potentiation methodology nerve cell nerve cell inhibition nerve tract physiology thalamus Animals Cerebral Cortex Drug Interactions Electroencephalography Membrane Potentials Mice, Inbred C57BL Neural Inhibition Neural Pathways Neurons Patch-Clamp Techniques Receptors, GABA-A Thalamus
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00063223_v66_n8_p769_Urbano http://hdl.handle.net/20.500.12110/paper_00063223_v66_n8_p769_Urbano
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	paper:paper_00063223_v66_n8_p769_Urbano2023-06-08T14:30:57Z Cocaine acute "binge" administration results in altered thalamocortical interactions in mice Cocaine GABA-A receptors Mice T-type calcium channels Thalamocortical dysrhythmia 2 amino 5 phosphonovaleric acid 4 aminobutyric acid A receptor 6 cyano 7 nitro 2,3 quinoxalinedione AMPA receptor antagonist calcium channel T type cesium cocaine kainic acid receptor antagonist n methyl dextro aspartic acid receptor blocking agent picrotoxin potassium ion tetrodotoxin 4 aminobutyric acid A receptor cocaine animal cell animal experiment animal model animal tissue article brain function brain slice cocaine dependence drug abuse electroencephalography in vitro study in vivo study mouse neurotransmitter release nonhuman patch clamp priority journal thalamocortical tract voltage clamp animal brain cortex C57BL mouse cell membrane potential drug antagonism drug effect drug interaction drug potentiation methodology nerve cell nerve cell inhibition nerve tract physiology thalamus Animals Cerebral Cortex Cocaine Drug Interactions Electroencephalography Membrane Potentials Mice Mice, Inbred C57BL Neural Inhibition Neural Pathways Neurons Patch-Clamp Techniques Receptors, GABA-A Thalamus Background: Abnormalities in both thalamic and cortical areas have been reported in human cocaine addicts with noninvasive functional magnetic resonance imaging. Given the substantial involvement of the thalamocortical system in sensory processing and perception, we defined electrophysiology-based protocols to attempt a characterization of cocaine effects on thalamocortical circuits. Methods: Thalamocortical function was studied in vivo and in vitro in mice after cocaine "binge" administration. In vivo awake electroencephalography (EEG) was implemented in mice injected with saline, 1 hour or 24 hours after the last cocaine "binge" injection. In vitro current- and voltage-clamp whole-cell patch-clamp recordings were performed from slices including thalamic relay ventrobasal (VB) neurons. Results: In vivo EEG recordings after cocaine "binge" administration showed a significant increment, compared with saline, in low frequencies while observing no changes in high-frequency γ activity. In vitro patch recordings from VB neurons after cocaine "binge" administration showed low threshold spikes activation at more negative membrane potentials and increments in both lh and low voltage activated T-type calcium currents. Also, a 10-mV negative shift on threshold activation level of T-type current and a remarkable increment in both frequency and amplitudes of γ-aminobutyric acid-A-mediated minis were observed. Conclusions: Our data indicate that thalamocortical dysfunctions observed in cocaine abusers might be due to two distinct but additive events: 1) increased low frequency oscillatory thalamocortical activity, and 2) overinhibition of VB neurons that can abnormally "lock" the whole thalamocortical system at low frequencies. © 2009 Society of Biological Psychiatry. 2009 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00063223_v66_n8_p769_Urbano http://hdl.handle.net/20.500.12110/paper_00063223_v66_n8_p769_Urbano
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Cocaine GABA-A receptors Mice T-type calcium channels Thalamocortical dysrhythmia 2 amino 5 phosphonovaleric acid 4 aminobutyric acid A receptor 6 cyano 7 nitro 2,3 quinoxalinedione AMPA receptor antagonist calcium channel T type cesium cocaine kainic acid receptor antagonist n methyl dextro aspartic acid receptor blocking agent picrotoxin potassium ion tetrodotoxin 4 aminobutyric acid A receptor cocaine animal cell animal experiment animal model animal tissue article brain function brain slice cocaine dependence drug abuse electroencephalography in vitro study in vivo study mouse neurotransmitter release nonhuman patch clamp priority journal thalamocortical tract voltage clamp animal brain cortex C57BL mouse cell membrane potential drug antagonism drug effect drug interaction drug potentiation methodology nerve cell nerve cell inhibition nerve tract physiology thalamus Animals Cerebral Cortex Cocaine Drug Interactions Electroencephalography Membrane Potentials Mice Mice, Inbred C57BL Neural Inhibition Neural Pathways Neurons Patch-Clamp Techniques Receptors, GABA-A Thalamus
spellingShingle	Cocaine GABA-A receptors Mice T-type calcium channels Thalamocortical dysrhythmia 2 amino 5 phosphonovaleric acid 4 aminobutyric acid A receptor 6 cyano 7 nitro 2,3 quinoxalinedione AMPA receptor antagonist calcium channel T type cesium cocaine kainic acid receptor antagonist n methyl dextro aspartic acid receptor blocking agent picrotoxin potassium ion tetrodotoxin 4 aminobutyric acid A receptor cocaine animal cell animal experiment animal model animal tissue article brain function brain slice cocaine dependence drug abuse electroencephalography in vitro study in vivo study mouse neurotransmitter release nonhuman patch clamp priority journal thalamocortical tract voltage clamp animal brain cortex C57BL mouse cell membrane potential drug antagonism drug effect drug interaction drug potentiation methodology nerve cell nerve cell inhibition nerve tract physiology thalamus Animals Cerebral Cortex Cocaine Drug Interactions Electroencephalography Membrane Potentials Mice Mice, Inbred C57BL Neural Inhibition Neural Pathways Neurons Patch-Clamp Techniques Receptors, GABA-A Thalamus Cocaine acute "binge" administration results in altered thalamocortical interactions in mice
topic_facet	Cocaine GABA-A receptors Mice T-type calcium channels Thalamocortical dysrhythmia 2 amino 5 phosphonovaleric acid 4 aminobutyric acid A receptor 6 cyano 7 nitro 2,3 quinoxalinedione AMPA receptor antagonist calcium channel T type cesium cocaine kainic acid receptor antagonist n methyl dextro aspartic acid receptor blocking agent picrotoxin potassium ion tetrodotoxin 4 aminobutyric acid A receptor cocaine animal cell animal experiment animal model animal tissue article brain function brain slice cocaine dependence drug abuse electroencephalography in vitro study in vivo study mouse neurotransmitter release nonhuman patch clamp priority journal thalamocortical tract voltage clamp animal brain cortex C57BL mouse cell membrane potential drug antagonism drug effect drug interaction drug potentiation methodology nerve cell nerve cell inhibition nerve tract physiology thalamus Animals Cerebral Cortex Cocaine Drug Interactions Electroencephalography Membrane Potentials Mice Mice, Inbred C57BL Neural Inhibition Neural Pathways Neurons Patch-Clamp Techniques Receptors, GABA-A Thalamus
description	Background: Abnormalities in both thalamic and cortical areas have been reported in human cocaine addicts with noninvasive functional magnetic resonance imaging. Given the substantial involvement of the thalamocortical system in sensory processing and perception, we defined electrophysiology-based protocols to attempt a characterization of cocaine effects on thalamocortical circuits. Methods: Thalamocortical function was studied in vivo and in vitro in mice after cocaine "binge" administration. In vivo awake electroencephalography (EEG) was implemented in mice injected with saline, 1 hour or 24 hours after the last cocaine "binge" injection. In vitro current- and voltage-clamp whole-cell patch-clamp recordings were performed from slices including thalamic relay ventrobasal (VB) neurons. Results: In vivo EEG recordings after cocaine "binge" administration showed a significant increment, compared with saline, in low frequencies while observing no changes in high-frequency γ activity. In vitro patch recordings from VB neurons after cocaine "binge" administration showed low threshold spikes activation at more negative membrane potentials and increments in both lh and low voltage activated T-type calcium currents. Also, a 10-mV negative shift on threshold activation level of T-type current and a remarkable increment in both frequency and amplitudes of γ-aminobutyric acid-A-mediated minis were observed. Conclusions: Our data indicate that thalamocortical dysfunctions observed in cocaine abusers might be due to two distinct but additive events: 1) increased low frequency oscillatory thalamocortical activity, and 2) overinhibition of VB neurons that can abnormally "lock" the whole thalamocortical system at low frequencies. © 2009 Society of Biological Psychiatry.
title	Cocaine acute "binge" administration results in altered thalamocortical interactions in mice
title_short	Cocaine acute "binge" administration results in altered thalamocortical interactions in mice
title_full	Cocaine acute "binge" administration results in altered thalamocortical interactions in mice
title_fullStr	Cocaine acute "binge" administration results in altered thalamocortical interactions in mice
title_full_unstemmed	Cocaine acute "binge" administration results in altered thalamocortical interactions in mice
title_sort	cocaine acute "binge" administration results in altered thalamocortical interactions in mice
publishDate	2009
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00063223_v66_n8_p769_Urbano http://hdl.handle.net/20.500.12110/paper_00063223_v66_n8_p769_Urbano
_version_	1768545031633764352

Cocaine acute "binge" administration results in altered thalamocortical interactions in mice

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