Nitric oxide regulates the firing rate of neuronal subtypes in the guinea pig ventral cochlear nucleus.
auditory system
central gain
neuromodulation
nitric oxide synthase
Journal
The European journal of neuroscience
ISSN: 1460-9568
Titre abrégé: Eur J Neurosci
Pays: France
ID NLM: 8918110
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
28
02
2019
revised:
20
08
2019
accepted:
29
08
2019
pubmed:
9
9
2019
medline:
22
6
2021
entrez:
9
9
2019
Statut:
ppublish
Résumé
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 subpopulation 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 neurones. 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 neurones 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.
Identifiants
pubmed: 31494975
doi: 10.1111/ejn.14572
pmc: PMC7078996
doi:
Substances chimiques
Enzyme Inhibitors
0
Nitric Oxide Donors
0
Nitric Oxide
31C4KY9ESH
NG-Nitroarginine Methyl Ester
V55S2QJN2X
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
963-983Subventions
Organisme : Medical Research Council
ID : MC_UU_00010/5
Pays : United Kingdom
Organisme : Medical Research Council
ID : RS_1595452
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_U135097126
Pays : United Kingdom
Informations de copyright
© 2019 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
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