RAPID COMMUNICATION GABAB Receptor-Mediated Modulation of Presynaptic Currents and Excitatory Transmission at a Fast Central Synapse

Isaacson, Jeffry S. GABAB receptor-mediated modulation of pre(Bennett and Ho 1991; Stanley and Mirotznick 1997; Yawo synaptic currents and excitatory transmission at a fast central synand Chuhma 1993). However, the small size of most synapapse. J. Neurophysiol. 80: 1571–1576, 1998. Large nerve termitic structures in the mammalian brain made direct electronals (calyces of Held) in the medial nucleus of the trapezoid body physiological studies of presynaptic terminals and their mod(MNTB) offer a unique opportunity to explore the modulation of ulation impossible. In mammals, single nerve fibers originatpresynaptic channels at a mammalian central synapse. In this study ing from bushy cells of the ventral cochlear nucleus make I examined g-aminobutyric acid-B (GABAB)-mediated presynapunusually large contacts ( the calyces of Held) onto the cell tic inhibition at the calyx of Held in slices of the rat auditory bodies of principal cells in the medial nucleus of the trapebrain stem. The selective GABAB agonist baclofen caused a potent zoid body (MNTB) (Barnes-Davies and Forsythe 1995; inhibition of synaptic transmission and presynaptic Ca current. The inhibition of presynaptic Ca channels was associated with Borst and Sakmann 1996; Takahashi et al. 1996). In this a slowing of the activation kinetics of the underlying current, and study, I used patch-clamp techniques to examine directly the the inhibition was relieved by strong depolarization. The inhibition actions of GABAB receptors on presynaptic channels in caof both synaptic transmission and presynaptic Ca current was lyx nerve terminals of the mammalian auditory brain stem. abolished by N-ethylmaleimide, a sulfhydryl alkylating agent that