Journal of Neuroscience, Vol 12, 3084-3097, Copyright © 1992 by Society for Neuroscience
Synaptic pharmacology of the superior olivary complex studied in mouse brain slice
SH Wu and JB Kelly
Psychology Department, Carleton University, Ottawa, Ontario, Canada.
The synaptic pharmacology of the lateral superior olive (LSO) and medial
nucleus of the trapezoid body (MNTB) was examined in a brain slice
preparation of the mouse superior olivary complex (SOC). Physiological
responses in SOC were elicited by electrical stimulation of the trapezoid
body ipsilateral or contralateral to the recording site, and bilateral
interactions were investigated by combined ipsilateral and contralateral
stimulation. Pharmacological effects were tested by bath application of
amino acid agonists and antagonists. Neurons in MNTB were excited by
contralateral stimulation and unaffected by ipsilateral stimulation.
Excitatory amino acid (EAA) agonists--kainic acid (KA), quisqualic acid
(QA), or L-glutamate-- caused spontaneous firing at low concentrations and
eliminated responses at higher concentrations in MNTB. The EAA agonist NMDA
had relatively little effect at comparable concentrations. Stimulus-
elicited responses were blocked by non-NMDA antagonists 6-cyano-7-
nitroquinoxaline-2,3-dione (CNQX) and 6,7-dinitro-quinoxaline-2,3-dione
(DNQX) and by the nonspecific EAA antagonist kynurenic acid, but were
unaffected by the NMDA antagonist D,L-2-amino-5-phosphonovaleric acid
(APV). LSO neurons were typically excited by ipsilateral stimulation and
inhibited by contralateral stimulation. In LSO, KA, QA, and L- glutamate
caused spontaneous firing at low concentrations and eliminated responses at
higher concentrations, and NMDA had relatively little effect. Excitatory
responses in the vast majority of LSO neurons were blocked by CNQX, DNQX,
or kynurenic acid. Some responses were also blocked by APV. LSO neurons
were affected by glycine, and contralateral inhibition in LSO was
completely blocked by strychnine. NMDA also blocked inhibition in LSO.
These results indicate that excitation of both MNTB and LSO neurons is
mediated primarily by an EAA neurotransmitter through non-NMDA receptors
and that contralateral inhibition of LSO cells is mediated through
strychnine-dependent glycine receptors. NMDA receptors may play a role in
binaural processing by modulating contralateral inhibitory input to LSO.
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