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Nitric oxide regulates the firing rate of neuronal subtypes in the guinea pig ventral cochlear nucleus

Hockley, Adam; Berger, Joel I.; Smith, Paul A.; Palmer, Alan R.; Wallace, Mark N.

Authors

Adam Hockley

Joel I. Berger

PAUL SMITH paul.a.smith@nottingham.ac.uk
Assistant Professor

Alan R. Palmer



Abstract

The gaseous free radical, nitric oxide (NO) acts as a ubiquitous neuromodulator, contributing to synaptic plasticity in a complex way that can involve either long term potentiation or depression. It is produced by neuronal nitric oxide synthase (nNOS) which is presynaptically expressed and also located postsynaptically in the membrane and cytoplasm of a sub-population of each major neuronal type in the ventral cochlear nucleus (VCN). We have used iontophoresis in vivo to study the effect of the NOS inhibitor L-NAME (L-NG-Nitroarginine methyl ester) and the NO donors SIN-1 (3-Morpholinosydnonimine hydrochloride) and SNOG (S-Nitrosoglutathione) on VCN units under urethane anaesthesia. Collectively, both donors produced increases and decreases in driven and spontaneous firing rates of some neurons. Inhibition of endogenous NO production with L-NAME evoked a consistent increase in driven firing rates in 18% of units without much effect on spontaneous rate. This reduction of gain produced by endogenous NO was mirrored when studying the effect of L-NAME on NMDA (N-Methyl-D-aspartic acid)-evoked excitation, with 30% of units showing enhanced NMDA-evoked excitation during L-NAME application (reduced NO levels). Approximately 25% of neurons contain nNOS and the NO produced can modulate the firing rate of the main principal cells: medium stellates (choppers), large stellates (onset responses) and bushy cells (primary like responses). The main endogenous role of NO seems to be to partly suppress driven firing rates associated with NMDA channel activity but there is scope for it to increase neural gain if there were a pathological increase in its production following hearing loss.

Citation

Hockley, A., Berger, J. I., Smith, P. A., Palmer, A. R., & Wallace, M. N. (2020). Nitric oxide regulates the firing rate of neuronal subtypes in the guinea pig ventral cochlear nucleus. European Journal of Neuroscience, 51(4), 963-983. https://doi.org/10.1111/ejn.14572

Journal Article Type Article
Acceptance Date Aug 29, 2019
Online Publication Date Oct 10, 2019
Publication Date 2020-02
Deposit Date Sep 3, 2019
Publicly Available Date Oct 11, 2020
Journal European Journal of Neuroscience
Print ISSN 0953-816X
Electronic ISSN 1460-9568
Publisher Wiley
Peer Reviewed Peer Reviewed
Volume 51
Issue 4
Pages 963-983
DOI https://doi.org/10.1111/ejn.14572
Keywords Cochlear nucleus, Nitric oxide synthase, Central gain, Auditory system
Public URL https://nottingham-repository.worktribe.com/output/2553068
Publisher URL https://onlinelibrary.wiley.com/doi/full/10.1111/ejn.14572

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Publisher Licence URL
http://creativecommons.org/licenses/by/4.0/





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