Calcium channels triggering transmitter release in the rat medial superior olive

We used whole cell voltage clamp recordings from neurones in rat auditory brainstem slices to study the Ca 2+ channel types involved in triggering synaptic glutamate and glycine release in the medial superior olivary nucleus. Glutamate release from the anterior ventral cochlear (aVCN) bushy neurone...

Full description

Saved in:
Bibliographic Details
Published inHearing research Vol. 162; no. 1; pp. 134 - 145
Main Authors Barnes-Davies, Margaret, Owens, Steven, Forsythe, Ian D.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 01.12.2001
Elsevier
Subjects
Rat
Online AccessGet full text

Cover

Loading…
More Information
Summary:We used whole cell voltage clamp recordings from neurones in rat auditory brainstem slices to study the Ca 2+ channel types involved in triggering synaptic glutamate and glycine release in the medial superior olivary nucleus. Glutamate release from the anterior ventral cochlear (aVCN) bushy neurone synapse did not involve L-type Ca 2+ channels (α 1C–D; Ca V1.2–1.3), but was mediated with similar efficacies by both N-type (α 1B; Ca V2.2) and the P/Q-type Ca 2+ channels (α 1A; Ca V2.1). Glycine release from the medial nucleus of the trapezoid body (MNTB) synapse was mediated predominantly by P/Q-type Ca 2+ channels, but with a significant contribution from N-type Ca 2+ channels. Combined application of the P/Q- and N-type Ca 2+ channel toxins, ω-agatoxin IVA and ω-conotoxin GVIA, left a very small remnant of both the inhibitory and excitatory postsynaptic currents, probably reflecting a minimal contribution of R-type Ca 2+ channels (α 1E; Ca V2.3) to transmitter release. In contrast with aVCN bushy neurones, MNTB somata lacked both T- (α 1G–I; Ca V3.1–3.3) and L-type channels, but expressed a higher proportion of P/Q-type Ca 2+ channels.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0378-5955
1878-5891
DOI:10.1016/S0378-5955(01)00378-1