RESPONSES OF CORTICAL NORADRENERGIC AND SOMATOSTINERGIC FIBERS AND TERMINALS TO ADJACENT STROKES AND SUBSEQUENT TREATMENT WITH NGF AND OR THE GANGLIOSIDE GM1/

The occurrence of sprouting by fibre systems in the neocortex followin g lesion is still a controversial issue, In previous studies, we showe d a nerve growth factor (NGF)-induced sprouting and hypertrophy of pre synaptic terminals in the cholinergic fibres of the rat neocortex foll owing stroke-type lesions, effects that were potentiated by the monosi aloganglioside GM1. The present study investigated whether exogenous N GF and/or GM1 treatment could also affect the noradrenergic and somato stinergic systems in the neocortex, Immediately following unilateral v ascular decortication, adult rats received, via minipump, a 7-day infu sion of vehicle, NGF (12 mu g/day) and/or GM1 (1.5 mg/day) into the ce rebroventricular space, Thirty days postlesion, the animals were perfu sed with histological fixatives, the brains were removed, and relevant sections were processed for dopamine beta-hydroxylase and somatostati n immunocytochemistry at the light and electron microscopic levels, A Quantimet 920 image analysis system was used for the quantification of fibre length and size of presynaptic boutons, The lesion caused a red uction in the dopamine beta-hydroxylase-immunoreactive fibre length, w hich was not attenuated by either NGF or GM1 treatment or both, The so matostatin-immunoreactive network, in contrast, was unaffected by the lesion, and there was no sprouting of somatostatin fibres following tr ophic factor therapy, We also found no significant differences in the size and number of synapses of both the dopamine beta-hydroxylase-immu noreactive and somatostatin-immunoreactive boutons following lesion an d drug treatments, These results indicate that NGF and/or GM1 therapie s do not cause regrowth in the noradrenergic and somatostatinergic cor tical fibre networks or their presynaptic elements following a cortica l devascularizing lesion. (C) 1997 Wiley-Liss, Inc.