Inhibitory synaptic transmission is of fundamental importance during t
he maturation of central auditory circuits, and their subsequent abili
ty to process acoustic information. The present study investigated the
manner in which inhibitory transmission regulates intracellular free
calcium levels in the gerbil inferior colliculus using a brain slice p
reparation. Inhibitory and excitatory postsynaptic potentials were evo
ked by electrical stimulation of the ascending afferents at the level
of the dorsal nucleus of the lateral lemniscus. Pharmacologically isol
ated inhibitory synaptic potentials were able to attenuate a calcium r
ise in collicular neurons that was generated by depolarizing current i
njection. In addition, GABA(A) and glycine receptor antagonists typica
lly led to an increase of calcium in collicular neurons during electri
cal stimulation of the ascending afferent pathway at the level of the
dorsal nucleus of the lateral lemniscus. Bath application of GABA or m
uscimol, a GABA(A) receptor agonist, evoked a brief hyperpolarization
followed by a long-lasting depolarization in inferior colliculus neuro
ns. This treatment also induced a transient calcium increase that corr
elated with the membrane depolarization phase. Baclofen, a GABA(B), re
ceptor agonist, had no effect on either membrane potential or calcium
levels. Ratiometric measures indicated that the muscimol-evoked rise i
n calcium was approximate to 150 nM above basal levels. The muscimol-e
voked responses were completely antagonized by bicuculline and attenua
ted by picrotoxin. Together, these results suggest that inhibitory syn
aptic transmission participates in the regulation of postsynaptic calc
ium during the developmental period. Inhibitory transmission may atten
uate a calcium influx that is evoked by excitatory synapses, but it ca
n also produce a modest influx of calcium when activated alone. These
mechanisms may help to explain the influence of inhibitory transmissio
n on the development of postsynaptic properties. (C) 1998 IBRO. Publis
hed by Elsevier Science Ltd.