DISTRIBUTION OF GAP-43 MESSENGER-RNA IN THE ADULT-RAT BRAIN

Regional distribution of gene expression of the axonal growth-associat ed protein, GAP-43, was studied in adult rat brains by in situ hybridi zation autoradiography to determine the features of mature neuronal po pulations that synthesize GAP-43 protein. Such synthesis appears to co rrelate with axonal growth during maturation and regrowth after axotom y. In most adult neurons, the sharp decline in GAP-43 gene expression implies a reduced capacity for axonal growth. Neurons capable of exten ding axonal knobs in the absence of injury may indicate a ''plasticity '' underlying dynamic processes of interaction between neurons and the ir synaptic targets. Antisense and sense (control) riboprobes were use d on serial sections in the three principal axes, and the magnitude of hybridization signal was examined to determine regional patterns. GAP -43 mRNA levels are pronounced in diverse neuronal groups including th e locus coeruleus, raphe nn., dopaminergic nigral and ventral tegmenta l nn., mitral cells, hippocampal CA3, inferior olivary n., vagal motor n. and other parasympathetic preganglionic neurons, select thalamic m idline and intralaminar nn., several specific nn. of the hypothalamus and basal forebrain, the granular layer of cerebellar cortex, the infr agranular neocortex, and the granular olfactory paleocortex; there is a substantial range in the magnitude of expression. Regions revealing minimal signal include most thalamic sensory relay nuclei, the granule neurons of the olfactory bulb and dentate gyrus, and the caudate and putamen. Possible concomitants of GAP-43 expression include regulation of ion flux and neurotransmitter release. Those neurons with long, ex tensively dispersed and numerous synaptic connections display the stro ngest signals and may possess the greatest propensity for continuous g rowth and turnover of their axon terminals, in contrast to short-axon and specific projection neurons exhibiting minimal levels. These data may enable inferring which populations display normal or experimentall y induced axonal growth. (C) 1993 Wiley-Liss, Inc.