Astrocytic iNOS-dependent enhancement of synaptic release in mouse neocortex

Yossi Buskila, Yael Amitai

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


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 Ca2+-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.

Original languageEnglish
Pages (from-to)1322-1328
Number of pages7
JournalJournal of Neurophysiology
Issue number3
StatePublished - 1 Mar 2010

ASJC Scopus subject areas

  • General Neuroscience
  • Physiology


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