Galanin systems and ischemia: peptide and receptor plasticity in neurons and oligodendroglial precursors.

Abstract

Cerebral cortex contains few if any galanin neurons, but receives galanin-ergic inputs from subcortical areas. Apart from our earlier study on the response to cortical spreading depression, little is known about the presence and function of galanin in normal or injured cortex and to gain more insight into its possible roles, we investigated the temporal effects of focal ischemia on the expression of galanin and galanin receptors (GalRs). Focal ischemia induced in the rat by unilateral middle cerebral artery occlusion increased galanin and GalR1 mRNAs in penumbral/undamaged areas on the first and second day post-ischemia, while increased GalR2 mRNA was observed in the same regions only on the second day. Immunohistochemical studies revealed galanin immunoreactive neurons in the frontal/ cingulate cortex and abundant galanin-immunoreactivity in nerve axons/fibres within the penumbral areas, between the third and the seventh day after ischemia. Galanin mRNA and immunoreactivity was also increased in a population of small cells thought to be NG2-positive oligodendrocyte precursors. Up-regulation of galanin and GalRs in various cell populations following severe ischemic injury further demonstrates the marked plasticity of galanin and GalR1/2 expression after brain injury, and together with data reported elsewhere in this volume, suggests a functional role for galanin signalling in such pathophysiological conditions.