PT  - JOURNAL ARTICLE
AU  - R A Travagli
AU  - M Ulivi
AU  - W J Wojcik
TI  - gamma-Aminobutyric acid-B receptors inhibit glutamate release from cerebellar granule cells: consequences of inhibiting cyclic AMP formation and calcium influx.
DP  - 1991 Sep 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 903--909
VI  - 258
IP  - 3
4099  - http://jpet.aspetjournals.org/content/258/3/903.short
4100  - http://jpet.aspetjournals.org/content/258/3/903.full
SO  - J Pharmacol Exp Ther1991 Sep 01; 258
AB  - In cerebellar granule cells, baclofen acted with micromolar concentrations at proposed gamma-aminobutyric acid-B receptors to inhibit the formation of cyclic AMP and depolarization-induced release of glutamate. Nanomolar concentrations of baclofen inhibited depolarization-induced influx of calcium. All three responses to baclofen were attenuated after pertussis toxin pretreatment of cell cultures. The inhibition of calcium influx and glutamate release were reversed by the cyclic AMP analog, 8-(4-chlorphenylthio)-cyclic AMP. The release of glutamate was dependent on the influx of extracellular calcium, which enters the cell through dihydropyridine-sensitive voltage-dependent calcium channels. Because the decrease in calcium influx by baclofen and nifedipine were additive, the baclofen-mediated decrease in calcium influx may not involve a dihydropyridine-sensitive calcium channel. These results show similarities between the baclofen-mediated inhibition of cyclic AMP formation and glutamate release, suggesting a relationship between these two events. The baclofen-mediated inhibition of calcium influx may not be related to baclofen's inhibition of glutamate release.