Synaptic Inputs to Stellate Cells in the Ventral Cochlear Nucleus.
Michael J. Ferragamo, Nace L. Golding, Donata Oertel.
Department of Neurophysiology, University of Wisconsin Medical School,
Madison, Wisconsin 53706-1532.
APStracts 4:187N, 1997.
ABSTRACT
Auditory information is carried from the cochlear nuclei to the inferior
colliculi through six parallel ascending pathways, one of which is through
stellate cells of the ventral cochlear nuclei (VCN) through the trapezoid
body. To characterize and identify the synaptic influences on T stellate
cells, intracellular recordings were made from anatomically identified
stellate cells in parasagittal slices of murine cochlear nuclei. Shocks to the
auditory nerve consistently evoked 5 types of synaptic responses in T stellate
cells which reflect sources intrinsic to the cochlear nuclear complex: (1)
Monosynaptic EPSPs that were blocked by 6,7-dinitroquinoxaline-2,3-dione
(DNQX), an antagonist of AMPA receptors, probably reflected activation by
auditory nerve fibers. Electrophysiological estimates indicate that about 5
auditory nerve fibers converge upon one T stellate cell. (2) Disynaptic,
glycinergic IPSPs arise through inhibitory interneurons in the VCN or in the
dorsal cochlear nucleus (DCN). (3) Slow depolarizations whose source has not
been identified that lasted between 0.2 and 1 sec and were blocked by DL-2-
amino-5-phosphonovaleric acid (APV), the NMDA receptor antagonist. (4) Rapid,
late glutamatergic EPSPs are polysynaptic and may arise from other T stellate
cells. (5) Trains of late glycinergic IPSPs after single or repetitive shocks
match the responses of D stellate cells, showing that D stellate cells are one
source of glycinergic inhibition to T stellate cells.
The source of late, polysynaptic EPSPs and IPSPs was assessed
electrophysiologically and pharmacologically. Late synaptic responses in T
stellate cells were enhanced by repetitive stimulation, indicating that the
interneurons from which they arose should fire trains of action potentials in
responses to trains of shocks. Late EPSPs and late IPSPs were blocked by APV
and enhanced by the removal of Mg2+ indicating that the interneurons were
driven at least in part through NMDA receptors. Bicuculline, a GABAa receptor
antagonist, enhanced the late PSPs, indicating that GABAergic inhibition
suppresses both the glycinergic interneurons responsible for the trains of
IPSPs in T-stellate cells and the interneuron responsible for late EPSPs in T
stellate cells. The glycinergic interneurons that mediate the series of IPSPs
are intrinsic to the ventral cochlear nucleus, because long series of IPSPs
were recorded from T stellate cells in slices in which the DCN was removed.
These experiments indicate that T stellate cells are a potential source of
late EPSPs and that D stellate cells are a potential source for trains of late
IPSPs.
Received 11 April 1997; accepted in final form 5 August 1997.
APS Manuscript Number J294-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 28 August 1997