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The Journal of Neurophysiology Vol. 87 No. 6 June 2002, pp. 2734-2740
Copyright ©2002 by the American Physiological Society
The Auditory Laboratory, Department of Physiology, The University of Western Australia, Crawley, Western Australia 6009, Australia
Robertson, Donald and
Bardia Paki.
Role of L-Type Ca2+ Channels in Transmitter Release
From Mammalian Inner Hair Cells. II. Single-Neuron Activity. J. Neurophysiol. 87: 2734-2740, 2002. Previously reported changes in the gross sound-evoked cochlear
potentials after intracochlear perfusion of nimodipine suggest that
dihydropyridine-sensitive Ca2+ channels (L-type)
control the sound-evoked release of transmitter from the inner hair
cells of the mammalian cochlea. In the present study, we combined
recording of the action potentials of single primary auditory afferent
neurons with intracochlear perfusion to further investigate the role of
voltage-gated Ca2+ channels at this synapse.
Spontaneous action potential firing rates were depressed by the L-type
channel blocker nimodipine, but were elevated by S(
) BAY
K8644, an L-type channel agonist. Sound-evoked responses of single
primary afferents were depressed by nimodipine in a manner that was
consistent with a block at the inner hair cell-afferent dendrite
synapse. Perfusions with solutions containing the N-type channel
blocker conotoxin GVIA did not differ in their effects from control
artificial perilymph perfusions. The results extend the conclusions of
the earlier study by showing that L-type Ca2+
channels are primarily responsible for controlling both spontaneous and
sound-evoked transmitter release from inner hair cells. In addition it
was found that afferent neurons with widely different spontaneous
firing rates were all sensitive to nimodipine and to BAY K8644,
suggesting that the multiple synaptic outputs of each inner hair cell
are under the control of only one major type of
Ca2+ channel.
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