γ-Aminobutyric acid-b receptors inhibit glutamate release from cerebellar granule cells: Consequences of inhibiting cyclic AMP formation and calcium influx

Renato Alberto Travagli, M. Ulivi, W. J. Wojcik

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Abstract

In cerebellar granule cells, baclofen acted with micromolar concentrations at proposed γ-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-chlorophenylthio)-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.

Original languageEnglish (US)
Pages (from-to)903-909
Number of pages7
JournalJournal of Pharmacology and Experimental Therapeutics
Volume258
Issue number3
StatePublished - Jan 1 1991

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Aminobutyrates
Baclofen
Glutamate Receptors
Cyclic AMP
Calcium
Glutamic Acid
Calcium Channels
Pertussis Toxin
Nifedipine
Cell Culture Techniques

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

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title = "γ-Aminobutyric acid-b receptors inhibit glutamate release from cerebellar granule cells: Consequences of inhibiting cyclic AMP formation and calcium influx",
abstract = "In cerebellar granule cells, baclofen acted with micromolar concentrations at proposed γ-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-chlorophenylthio)-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.",
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AU - Travagli, Renato Alberto

AU - Ulivi, M.

AU - Wojcik, W. J.

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N2 - In cerebellar granule cells, baclofen acted with micromolar concentrations at proposed γ-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-chlorophenylthio)-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.

AB - In cerebellar granule cells, baclofen acted with micromolar concentrations at proposed γ-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-chlorophenylthio)-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.

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