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Responses of cortical noradrenergic and somatostinergic fibres and terminals to adjacent strokes and subsequent treatment with NGF and/or the ganglioside GM1
Author(s) -
Tajrine Dima,
Garofalo Lorella,
Cuello A. Claudio,
RibeirodaSilva Alfredo
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19971115)50:4<627::aid-jnr13>3.0.co;2-#
Subject(s) - somatostatin , neocortex , lesion , dopamine , endocrinology , medicine , nerve growth factor , sprouting , biology , neuroscience , pathology , receptor , botany
The occurrence of sprouting by fibre systems in the neocortex following lesion is still a controversial issue. In previous studies, we showed a nerve growth factor (NGF)‐induced sprouting and hypertrophy of presynaptic terminals in the cholinergic fibres of the rat neocortex following stroke‐type lesions, effects that were potentiated by the monosialoganglioside GM1. The present study investigated whether exogenous NGF and/or GM1 treatment could also affect the noradrenergic and somatostinergic systems in the neocortex. Immediately following unilateral vascular decortication, adult rats received, via minipump, a 7‐day infusion of vehicle, NGF (12 μg/day) and/or GM1 (1.5 mg/day) into the cerebroventricular space. Thirty days postlesion, the animals were perfused with histological fixatives, the brains were removed, and relevant sections were processed for dopamine β‐hydroxylase and somatostatin 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 reduction in the dopamine β‐hydroxylase‐immunoreactive fibre length, which was not attenuated by either NGF or GM1 treatment or both. The somatostatin‐immunoreactive network, in contrast, was unaffected by the lesion, and there was no sprouting of somatostatin fibres following trophic factor therapy. We also found no significant differences in the size and number of synapses of both the dopamine β‐hydroxylase‐immunoreactive and somatostatin‐immunoreactive boutons following lesion and drug treatments. These results indicate that NGF and/or GM1 therapies do not cause regrowth in the noradrenergic and somatostatinergic cortical fibre networks or their presynaptic elements following a cortical devascularizing lesion. J. Neurosci. Res. 50:627–642, 1997. © 1997 Wiley‐Liss, Inc.