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Paradoxical Facilitation of the Voltage-Dependent Calcium Current Following Activation of GABAB Receptors

Nobukuni Ogata, S. Fujikawa, Haruhiko Motomura

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Abstract

The mechanisms underlying the enhancement of the calcium current (ICa) after application of baclofen, a GABAB agonist, were studied in neurons of the rat dorsal root ganglia using nystatin perforated patch clamp recording. Baclofen (50 μM) decreased ICa and slowed the onset of ICa. However, when baclofen was rapidly washed out from the medium, the amplitude of ICa was paradoxically augmented exceeding the control value measured before application of the drug. This enhancement of ICa by baclofen was not due to desensitization of GABAB receptors or a liberation from tonic G protein-mediated inhibition of ICa. From its extremely prolonged time course, an involvement of some intracellular signal transduction system was strongly suggested.

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What this paper is about

The mechanisms underlying the enhancement of the calcium current (ICa) after application of baclofen, a GABAB agonist, were studied in neurons of the rat dorsal root ganglia using nystatin perforated patch clamp recording. Baclofen (50 μM) decreased ICa and slowed the onset of ICa. However, when baclofen was rapidly washed out from the medium, the amplitude of ICa was paradoxically augmented exceeding the control value measured before application of the drug. This enhancement of ICa by baclofen was not due to desensitization of GABAB receptors or a liberation from tonic G protein-mediated inhibition of ICa. From its extremely prolonged time course, an involvement of some intracellular signal transduction system was strongly suggested.

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Available abstract

The mechanisms underlying the enhancement of the calcium current (ICa) after application of baclofen, a GABAB agonist, were studied in neurons of the rat dorsal root ganglia using nystatin perforated patch clamp recording. Baclofen (50 μM) decreased ICa and slowed the onset of ICa. However, when baclofen was rapidly washed out from the medium, the amplitude of ICa was paradoxically augmented exceeding the control value measured before application of the drug. This enhancement of ICa by baclofen was not due to desensitization of GABAB receptors or a liberation from tonic G protein-mediated inhibition of ICa. From its extremely prolonged time course, an involvement of some intracellular signal transduction system was strongly suggested.

Key concepts: Baclofen, GABAB receptor, Agonist, Desensitization (medicine), Neuroscience, Chemistry, Tonic (physiology), Receptor

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