NDLI: Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.

Please wait, while we are loading the content...

Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Läck, A. K. Christian, D. T. Diaz, M. R. McCool, B. A.
Description	Country affiliation: United States Author Affiliation: Läck AK ( Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.)
Abstract	Withdrawal (WD) anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is extensive, long-lasting, and develops well after the obvious physical symptoms of acute WD. The neurobiological mechanisms underlying this prolonged WD-induced anxiety are not well understood. The basolateral amygdala (BLA) is a major emotional center in the brain and regulates the expression of anxiety. New evidence suggests that increased glutamatergic function in the BLA may contribute to WD-related anxiety following chronic ethanol exposure. Recent evidence also suggests that kainate-type ionotropic glutamate receptors are inhibited by intoxicating concentrations of acute ethanol. This acute sensitivity suggests potential (KA-R) contributions by these receptors to the increased glutamatergic function seen during chronic exposure. Therefore, we examined the effect of chronic intermittent ethanol (CIE) and WD on KA-R-mediated synaptic transmission in the BLA of Sprague-Dawley rats. Our study showed that CIE, but not WD, increased synaptic responses mediated by KA-Rs. Interestingly, both CIE and WD occluded KA-R-mediated synaptic plasticity. Finally, we found that BLA field excitatory postsynaptic potential responses were increased during CIE and WD via a mechanism that is independent of glutamate release from presynaptic terminals. Taken together, these data suggest that KA-Rs might contribute to postsynaptic increases in glutamatergic synaptic transmission during CIE and that the mechanisms responsible for the expression of KA-R-dependent synaptic plasticity might be engaged by chronic ethanol exposure and WD.
File Format	HTM / HTML
ISSN	07418329
e-ISSN	18736823
DOI	10.1016/j.alcohol.2008.11.002
Journal	Alcohol
Issue Number	1
Volume Number	43
Language	English
Publisher	Elsevier
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Substance-Related Disorders Amygdala Drug Effects Central Nervous System Depressants Pharmacology Ethanol Receptors, Kainic Acid Substance Withdrawal Syndrome Physiopathology Synaptic Transmission Alanine Analogs & Derivatives Animals Brain Pathology Electric Stimulation Electrophysiology Excitatory Postsynaptic Potentials Neuronal Plasticity Patch-clamp Techniques Rats, Sprague-dawley Receptors, Glutamate Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Neurology Medicine Behavioral Neuroscience Health (social science) Biochemistry Toxicology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

D-cycloserine facilitates synaptic plasticity but impairs glutamatergic neurotransmission in rat hippocampal slices.

Glutamate released spontaneously from astrocytes sets the threshold for synaptic plasticity

Protein kinase Cγ mediates ethanol withdrawal hyper-responsiveness of NMDA receptor currents in spinal cord motor neurons

Sustained ethanol inhibition of native AMPA receptors on medial septum/diagonal band (MS/DB) neurons.

Surface mobility of postsynaptic AMPARs tunes synaptic transmission.

Immature hippocampal neuronal networks do not develop tolerance to the excitatory actions of ethanol.

Ethanol-Induced Plasticity of GABAA Receptors in the Basolateral Amygdala

CHRONIC ETHANOL AND WITHDRAWAL EFFECTS ON KAINATE RECEPTOR-MEDIATED EXCITATORY NEUROTRANSMISSION IN THE RAT BASOLATERAL AMYGDALA

Ethanol disrupts NMDA receptor and astroglial EAAT2 modulation of Kv2.1 potassium channels in hippocampus

Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.

Similar Documents

D-cycloserine facilitates synaptic plasticity but impairs glutamatergic neurotransmission in rat hippocampal slices.

Glutamate released spontaneously from astrocytes sets the threshold for synaptic plasticity

Protein kinase Cγ mediates ethanol withdrawal hyper-responsiveness of NMDA receptor currents in spinal cord motor neurons

Sustained ethanol inhibition of native AMPA receptors on medial septum/diagonal band (MS/DB) neurons.

Surface mobility of postsynaptic AMPARs tunes synaptic transmission.

Immature hippocampal neuronal networks do not develop tolerance to the excitatory actions of ethanol.

Ethanol-Induced Plasticity of GABAA Receptors in the Basolateral Amygdala

CHRONIC ETHANOL AND WITHDRAWAL EFFECTS ON KAINATE RECEPTOR-MEDIATED EXCITATORY NEUROTRANSMISSION IN THE RAT BASOLATERAL AMYGDALA

Ethanol disrupts NMDA receptor and astroglial EAAT2 modulation of Kv2.1 potassium channels in hippocampus

Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.