Skip Navigation



Cerebral Cortex Advance Access published online on October 18, 2006
Cerebral Cortex, doi:10.1093/cercor/bhl096
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
17/8/1877    most recent
bhl096v1
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 Huang, C.-C.
Right arrow Articles by Hsu, K.-S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huang, C.-C.
Right arrow Articles by Hsu, K.-S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Article

Repeated Cocaine Administration Promotes Long-Term Potentiation Induction in Rat Medial Prefrontal Cortex

Chiung-Chun Huang 1, Hsiao-Ju Lin 1, and Kuei-Sen Hsu 2 *

1 Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan
2 Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Center for Gene Regulation and Signal Transduction Research, National Cheng Kung University, Tainan 701, Taiwan

* To whom correspondence should be addressed.
Kuei-Sen Hsu, E-mail: richard{at}mail.ncku.edu.tw


  Abstract

Although drug-induced adaptations in the prefrontal cortex (PFC) may contribute to several core aspects of addictive behaviors, it is not clear yet whether drugs of abuse elicit changes in synaptic plasticity at the PFC excitatory synapses. Here we report that, following repeated cocaine administration (15 mg/kg/day intraperitoneal injection for 5 consecutive days) with a 3-day withdrawal, excitatory synapses to layer V pyramidal neurons in rat medial prefrontal cortex (mPFC) become highly sensitive to the induction of long-term potentiation (LTP) by repeated correlated presynaptic and postsynaptic activity. This promoted LTP induction is caused by cocaine-induced reduction of {gamma}-aminobutyric acid (GABA)A receptor-mediated inhibition of mPFC pyramidal neurons. In contrast, in slices from rats treated with saline or a single dose of cocaine, the same LTP induction protocol did not induce significant LTP unless the blockade of GABAA receptors. Blockade of the D1-like receptors specifically prevented the cocaine-induced enhancement of LTP. Repeated cocaine exposure reduced the GABAA receptor-mediated synaptic currents in mPFC pyramidal neurons. Biotinylation experiments revealed a significant reduction of surface GABAA receptor {alpha}1 subunit expression in mPFC slices from repeated cocaine-treated rats. These findings support an important role for cocaine-induced enhancement of synaptic plasticity in the PFC in the development of drug-associated behavioral plasticity.

Keywords: addiction; cocaine; GABAA receptor; long-term potentiation; medial prefrontal cortex.
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. Neurosci.Home page
H. Lu, B. Lim, and M.-m. Poo
Cocaine Exposure In Utero Alters Synaptic Plasticity in the Medial Prefrontal Cortex of Postnatal Rats
J. Neurosci., October 7, 2009; 29(40): 12664 - 12674.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
B. Pan, C. J. Hillard, and Q.-s. Liu
Endocannabinoid Signaling Mediates Cocaine-Induced Inhibitory Synaptic Plasticity in Midbrain Dopamine Neurons
J. Neurosci., February 6, 2008; 28(6): 1385 - 1397.
[Abstract] [Full Text] [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.