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Volume 17, Number 3, Issue of February 1, 1997 pp. 1025-1032
Copyright ©1997 Society for Neuroscience

GABA_B Receptor-Mediated Inhibition of Tetrodotoxin-Resistant GABA Release in Rodent Hippocampal CA1 Pyramidal Cells

Received Nov. 14, 1996; accepted Nov. 25, 1996.

Wolfgang Jarolimek and Ulrich Misgeld

Institute of Physiology, University of Heidelberg, D-69120 Heidelberg, Germany

Tight-seal whole-cell recordings from CA1 pyramidal cells of rodent hippocampus were performed to study GABA_B receptor-mediated inhibition of tetrodotoxin (TTX)-resistant IPSCs. IPSCs were recorded in the presence of TTX and glutamate receptor antagonists. (R)-()-baclofen reduced the frequency of TTX-resistant IPSCs by a presynaptic action. The inhibition by (R)-()-baclofen was concentration-dependent, was not mimicked by the less effective enantiomer (S)-(+)-baclofen, and was blocked by the GABA_B receptor antagonist CGP 55845A, suggesting a specific effect on GABA_B receptors. The inhibition persisted in the presence of the Ca²⁺ channel blocker Cd²⁺. There was no requirement for an activation of K⁺ conductances by (R)-()-baclofen, because the inhibition of TTX-resistant IPSCs persisted in Ba²⁺ and Cd²⁺. Because the time courses of TTX-resistant IPSCs were not changed by (R)-()-baclofen, there was no evidence for a selective inhibition of quantal release from a subgroup of GABAergic terminals. (R)-()-baclofen reduced the frequency of TTX-resistant IPSCs in guinea pigs and Wistar rats, whereas the inhibition was much smaller in Sprague Dawley rats. In Cd²⁺ and Ba²⁺, -phorbol-12,13-dibutyrate and forskolin enhanced the frequency of TTX-resistant IPSCs. Only -phorbol-12,13-dibutyrate reduced the inhibition by (R)-()-baclofen. We conclude that GABA_B receptors inhibit TTX-resistant GABA release through a mechanism independent from the well known effects on Ca²⁺ or K⁺ channels. The inhibition of quantal GABA release can be reduced by an activator of protein kinase C.

Key words: GABA; baclofen; GABA_B receptors; quantal release; protein kinase C; adenylate cyclase; presynaptic; miniature IPSCs

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