Development of central control of adrenal catecholamine biosynthesis and release
In the mature rat, sympatho-adrenal Stressors evoke release of catecholamines from the adrenal medulla accompanied by stimulation of activity of catecholamine biosynthetic enzymes; both processes are controlled transsynaptically by impulses arising in the central nervous system. In the neonatal rat, drugs which ordinarily elicit sympatho-adrenal reflexes do not evoke neurally-mediated release and do not induce tyrosine hydroxylase or dopamine beta-hydroxylase, despite the fact that the central nervous system senses the stimuli and sends impulses down sympathetic preganglionic neurons; reflex responses first appear toward the end of the first week of postnatal life and are fully mature by 10 days of age. Since the immature adrenal medulla is capable of secreting catecholamines and inducing tyrosine hydroxylase in response to direct stimulation (nicotine), the initial lack of response to reflex stimulators probably results from immaturity of splanchnic nerve synaptic connections to the tissue. Despite the absence of functional neuronal connections, the neonatal adrenal is not entirely passive to all stressful stimuli, but instead is capable of releasing catecholamines by a non-neurogenic mechanism which is not present in mature rats. The non-neurogenic secretion may be modulated by opiate mechanisms, as release is potentiated by naloxone and reduced by methadone pretreatment. © 1982.
Slotkin, TA; Chantry, CJ; Bartolome, J
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