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By Sudarshan K. Malhotra

A part of a sequence which goals to hide fresh wisdom within the box of neural technology, this quantity discusses such subject matters as: the molecular bases of nerve regeneration; plasticity of descending spinal pathways in constructing mammals; and improvement of the mammalian auditory hindbrain.

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1988). D. , 1987), very little is known ontogenetically. , 1984; Palacios and Kuhar, 1981). Two distinct NT-binding sites have been identified in the rat forebrain: the NT 1 acceptor site (levobastine-sensitive) and the NT 2 receptor site (Schotte and Laduron, 1987). In the rat brain, NT 2 receptors are present at birth, reach maximum level on P10, and plateau at a lower lever in the adult. NT 1 receptors are not detected before P 10 and reach maximum levels at P30. Again, the high expression of NT 1 receptors early in the postnatal period may be associated with neuronal maturation.

Although in this review we have not discussed neurokinin B, another peptide of the tachykinin family (Maggio, 1988), it is of interest to note the coexpression of neurokinin B and SP genes in a subset of neurons in the rat habenula (Burgunder and Young, 1989); moreover, these peptides are also colocalized with CHAT. , 1987). Again, no studies are yet available on such interrelationships during ontogenesis. B. Neurotrophic Role of Neuropeptides As we have discussed throughout this review, the presence of neuropeptides and their receptors during early embryogenesis, and their colocalization with neurotransmitter substances, at least as documented in the adult CNS, are supportive evidence that these endogenous substances may be another set of growth factors with several of the functions attributed to the classical growth factors, including neuronal survival, neuronal growth, and neuronal phenotypic expression.

1984). , 1986). , 1988). On the other hand, Brenneman and Foster (1987) have reported that GHRH significantly reduces the survival of spinal cord neurons in culture. In contrast, our data suggest that the effect of GHRH administered to chick embryos during a critical period of neuroembryogenesis, from E 1 to E3, may enhance the survival of catecholaminergic neurons in the brain, the increased viability being reflected as an increase in TH activity. The apparent discrepancy between our findings and those of Brenneman and Foster may reflect the difference between the in vivo and in vitro systems.

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