By Sudarshan K. Malhotra
A part of a sequence which goals to hide contemporary wisdom within the box of neural technology, this quantity discusses such issues 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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Of interest is their finding that in DRG removed from 15-day-old chick embryos, nerve growth factor fails to cause a further increase. MacLean et al. (1988), using dissociated cultures of rat nodose ganglia, found that whereas nerve growth factor does not alter neuronal survival, SP content is doubled in the presence of nerve growth factor. In subsequent studies, plating of neurons onto previously dissociated rat atrocytes (for target cells) increased survival by 50% but did not alter SP content in surviving neurons.
Depolarizing agents, T-interferon, glucorticoid hormones, and prostaglandin synthesis inhibitors (indomethacin) all diminish the induction of SP and preprotachykinin mRNA by IL-1. In another study Jonakait and Schotland (1990) found that factor(s) released from Con A-stimulated splenocytes raises SP levels in cultured sympathetic ganglion cells. Thus they suggest, based on these two studies, that IL-1 may be one molecule active in the medium conditioned by splenocytes. The authors finally conclude that since SP has stimulatory effects on the immune system (several references in this article), the IL-1induced increase in ganglionic SP may be one means by which the nerves and immune systems interact during an acute ganglionic injury.
They conclude that in late pregnancy and lactation the expression of both neuropeptide genes is stimulated in parallel by mechanisms Neuropeptides in Development 19 operating at a pretranslational level, involving increased gene transcription or mRNA stabilization or both. , 1986). A decrease in this particular class of steroid (after adrenalectomy) appears to increase the potential for altering the expression of the propressophysin gene within this nucleus. , 1988) found that adrenalectomyinduced plasticity in VP expression is further enhanced by ablation of a specific afferent pathway.