Skip Navigation



Alcohol and Alcoholism Advance Access published online on February 16, 2006
Alcohol and Alcoholism, doi:10.1093/alcalc/agl006
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
41/4/379    most recent
agl006v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by MIGUEL-HIDALGO, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by MIGUEL-HIDALGO, J. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the Medical Council on Alcohol. All rights reserved
Received September 2, 2005
Revised December 29, 2005
Accepted January 16, 2006

Article

WITHDRAWAL FROM FREE-CHOICE ETHANOL CONSUMPTION RESULTS IN INCREASED PACKING DENSITY OF GLUTAMINE SYNTHETASE-IMMUNOREACTIVE ASTROCYTES IN THE PRELIMBIC CORTEX OF ALCOHOL-PREFERRING RATS

JOSÉ JAVIER MIGUEL-HIDALGO 1 *

1 Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS 39216, USA

* To whom correspondence should be addressed.
JOSÉ JAVIER MIGUEL-HIDALGO, E-mail: jmiguel-hidalgo{at}psychiatry.umsmed.edu


  Abstract

Excess activation of glutamatergic neurotransmission in the cerebral cortex following ethanol withdrawal is considered to contribute to significant behavioural disturbances, and to alcohol craving. Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to glutamine through the enzyme glutamine synthetase (GS). However, it is unclear if withdrawal from free-choice ethanol drinking causes changes in the numbers of astrocytes expressing GS or the cytoskeletal protein of astrocytes glial fibrillary acidic protein (GFAP). Alcohol-preferring (P) rats exposed to free-choice ethanol drinking were either maintained without forced interruption of ethanol drinking, subjected to a 3-day withdrawal period at the end of 2 months, or subjected to three 3-day withdrawal periods along 6 months. At 2 months, P rats were also compared with alcohol-naïve alcohol non-preferring rats (NP) rats. Packing density of GS and GFAP-immunoreactive (IR) astrocytes was measured in sections from the prelimbic cortex (PLC) using the optical disector probe. An alcohol deprivation effect was observed in P rats with withdrawals during a 6-month ethanol drinking. Ethanol withdrawal significantly increased the packing density of GS- and GFAP-IR astrocytes in the PLC of P rats as compared with P rats with continuous access to ethanol. In addition, there was a positive correlation between the pre-withdrawal ethanol consumption and the packing density of GS-IR astrocytes. The present results suggest the involvement of astrocytes in the regulation of the glutamatergic activation associated with withdrawal from free-choice ethanol consumption and point to differential adaptations of GS and GFAP to prolonged alcohol drinking in the PLC of P rats.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J PsychopharmacolHome page
J Miguel-Hidalgo, Y Shoyama, and V Wanzo
Infusion of gliotoxins or a gap junction blocker in the prelimbic cortex increases alcohol preference in Wistar rats
J Psychopharmacol, July 1, 2009; 23(5): 550 - 557.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.