Astrocytic iNOS-dependent enhancement of synaptic release in mouse neocortex.

Abstract:

:Nitric oxide (NO) has been recognized as an atypical neuronal messenger affecting synaptic transmission, but its cellular source has remained unresolved as the neuronal NO synthase isoform (nNOS) in brain areas such as the neocortex is expressed only by a small subset of inhibitory neurons. The involvement of the glial NOS isoform (iNOS) in modulating neuronal activity has been largely ignored because it has been accepted that this enzyme is regulated by gene induction following detrimental stimuli. Using acute brain slices from mouse neocortex and electrophysiology, we found that selective inhibition of iNOS reduced both spontaneous and evoked synaptic release. Moreover, iNOS inhibition partially prevented and reversed the potentiation of excitatory synapses in layer 2/3 pyramidal neurons. NOS enzymatic assay confirmed a small but reliable Ca(2+)-independent activity fraction, consistent with the existence of functioning iNOS in the tissue. Together these data point to astrocytes as a source for the nitrosative regulation of synaptic release in the neocortex.

journal_name

J Neurophysiol

authors

Buskila Y,Amitai Y

doi

10.1152/jn.00676.2009

subject

Has Abstract

pub_date

2010-03-01 00:00:00

pages

1322-8

issue

3

eissn

0022-3077

issn

1522-1598

pii

00676.2009

journal_volume

103

pub_type

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