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Summary: G-Protein-Coupled Modulation of Presynaptic Calcium Currents
and Transmitter Release by a GABAB Receptor
Tomoyuki Takahashi, Yoshinao Kajikawa, and Tetsuhiro Tsujimoto
Department of Neurophysiology, University of Tokyo Faculty of Medicine, Tokyo 113, Japan
Presynaptic GABAB receptors play a regulatory role in central
synaptic transmission. To elucidate their underlying mechanism
of action, we have made whole-cell recordings of calcium and
potassium currents from a giant presynaptic terminal, the calyx
of Held, and EPSCs from its postsynaptic target in the medial
nucleus of the trapezoid body of rat brainstem slices. The
GABAB receptor agonist baclofen suppressed EPSCs and pre-
synaptic calcium currents but had no effect on voltage-
dependent potassium currents. The calcium currentEPSC re-
lationship measured during baclofen application was similar to
that observed on reducing [Ca2
]o , suggesting that the pre-
synaptic inhibition generated by baclofen is caused largely by
the suppression of presynaptic calcium influx. Presynaptic
loading of the GDP analog guanosine-5 -O-(2-thiodiphosphate)
(GDP S) abolished the effect of baclofen on both presynaptic
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