![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 280, Issue 1, 129-137, 1997
-Aminobutyric Acid and Glutamate
Release by Altering Presynaptic and not Postsynaptic -Aminobutyric
AcidB Receptors within the Rat Dorsolateral Septal
Nucleus1
Department of Pharmacology and Toxicology, University of Texas
Medical Branch at Galveston, Galveston, Texas
Cocaine is a popular and sometimes deadly drug of abuse. Its mechanisms
of action have previously not been linked with receptors localized to
presynaptic sites for the major central nervous system amino acid
transmitters 
-aminobutyric acid (GABA) and glutamate. We demonstrate
that, within the dorsolateral septal nucleus of in vitro
brain slices from animals that had received cocaine chronically in vivo for 14 or 28, but not 7, days, control of both
inhibitory (GABA) and excitatory (glutamate) amino acid transmission is
impaired, due to the combined diminished effectiveness of presynaptic
GABAB auto- and heteroreceptors. As a result, disinhibition
of inhibitory and excitatory transmitters occurs, with enhanced
transmitter release. Although the involvement of postsynaptic
GABAB receptors has been suggested in the chronic actions
of cocaine at other central nervous system nuclei, we do not see any
change in the effectiveness of the postsynaptic GABAB
receptors within the dorsolateral septal nucleus. Modulation of
presynaptic GABAB receptors at central nervous system nerve
terminals after chronic cocaine administration has not been reported
previously. Our findings demonstrate that chronic intermittent cocaine
administration for at least 14 days induces a persistent change in
neuronal activity that involves both inhibitory and excitatory amino
acid-mediated transmission within the dorsolateral septal nucleus.
These results suggest that nerve terminal GABAB receptors
have been overlooked as playing a role in either the etiology and
treatment of chronic cocaine addiction or cocaine toxicity.
This article has been cited by other articles:
|
|
 |
|
  J. Liu, B. Yu, L. Orozco-Cabal, D. E. Grigoriadis, J. Rivier, W. W. Vale, P. Shinnick-Gallagher, and J. P. Gallagher Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2 Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum J. Neurosci., January 19, 2005; 25(3): 577 - 583. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z.-X. Xi, S. Ramamoorthy, H. Shen, R. Lake, D. J. Samuvel, and P. W. Kalivas GABA Transmission in the Nucleus Accumbens Is Altered after Withdrawal from Repeated Cocaine J. Neurosci., April 15, 2003; 23(8): 3498 - 3505. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Neugebauer, F. Zinebi, R. Russell, J. P. Gallagher, and P. Shinnick-Gallagher Cocaine and Kindling Alter the Sensitivity of Group II and III Metabotropic Glutamate Receptors in the Central Amygdala J Neurophysiol, August 1, 2000; 84(2): 759 - 770. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Yamada, B. Yu, and J. P. Gallagher Different Subtypes of GABAB Receptors Are Present at Pre- and Postsynaptic Sites Within the Rat Dorsolateral Septal Nucleus J Neurophysiol, June 1, 1999; 81(6): 2875 - 2883. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Shoji, D. Simms, K. Yamada, and J. P. Gallagher Cocaine Administered in Vitro to Brain Slices from Rats Treated with Cocaine Chronically in Vivo Results in a gamma -Aminobutyric Acid Receptor-Mediated Hyperpolarization Recorded from the Dorsolateral Septum J. Pharmacol. Exp. Ther., July 1, 1998; 286(1): 509 - 518. [Abstract] [Full Text]
|
|
|
|
|
|
X.-F. Zhang, X.-T. Hu, and F. J. White Whole-Cell Plasticity in Cocaine Withdrawal: Reduced Sodium Currents in Nucleus Accumbens Neurons J. Neurosci., January 1, 1998; 18(1): 488 - 498. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
