MolPharm xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kamatchi, G. L.
Right arrow Articles by Ticku, M. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kamatchi, G. L.
Right arrow Articles by Ticku, M. K.

Functional coupling of presynaptic GABAB receptors with voltage-gated Ca2+ channel: regulation by protein kinases A and C in cultured spinal cord neurons

GL Kamatchi and MK Ticku

Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764.

Depolarization-induced 86Rb efflux, an index of K+ efflux, was developed by using mammalian cultured spinal cord neurons to study the effect of gamma aminobutyric acid (GABAB) receptor activation on Ca2(+)- activated K(+)-channels. The Ca2(+)-activated 86Rb efflux was obtained by using two methods. The first method utilized depolarizing concentrations of KCl (100 mM) to study the voltage-gated Ca2+ channel activation, whereas in the second method, calcium ionophore A23187 was used to get the voltage-independent Ca2(+)-activated 86Rb efflux. The GABAB receptor agonist baclofen inhibited the efflux induced by depolarization but not by A23187, whereas tricyclic antidepressant desipramine inhibited the efflux induced by both depolarization and A23187. These results suggest that the GABAB receptor activation inhibits 86Rb efflux by inhibiting the voltage-gated Ca2+ channels. Moreover, forskolin and the analogs of cAMP antagonized the action of baclofen, suggesting that the GABAB receptors are negatively coupled to adenylate cyclase. Furthermore, protein kinase C activators antagonized this action of baclofen, while the antagonists of protein kinase C reversed their action on baclofen. In addition, the inactive forskolin, 1,9-dideoxyl forskolin, and the inactive phorbol analog, phorbol 12,13- didecanoate, did not influence the action of baclofen. Thus, it is suggested that the GABAB receptor activation inhibited the voltage- gated Ca2+ influx and that this action is under modulatory control by kinases A and C.

Volume 38, Issue 3, pp. 342-347, 09/01/1990
Copyright © 1990 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 J. Neurosci.Home page
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]

Home page
 Physiol. Rev.Home page
J. C. Rekling, G. D. Funk, D. A. Bayliss, X.-W. Dong, and J. L. Feldman
Synaptic Control of Motoneuronal Excitability
Physiol Rev, April 1, 2000; 80(2): 767 - 852.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1990 by the American Society for Pharmacology and Experimental Therapeutics