PERIPHERAL CHEMOSENSITIVITY AND CENTRAL INTEGRATION - NEUROPLASTICITYOF CATECHOLAMINERGIC CELLS UNDER HYPOXIA

The plasticity of catecholaminergic cells within the carotid body, bra instem and sympatho-adrenal system was analyzed in rats subjected to n ormobaric hypoxia (10% O-2) lasting up to 3 weeks. Long term hypoxia e licited structural, neurochemical and phenotypic changes in carotid bo dy and sympathetic ganglia (SIF cells), and stimulated the norepinephr ine turnover in A2 neurons located caudal to the obex, the area where the chemosensory nerve fibers end. Chemodenervation abolished central alterations. Adaptive mechanisms for increasing norepinephrine biosynt hesis in hypoxia involved changes in activity of pre-existing tyrosine hydroxylase, the rate-limiting enzyme of catecholamine biosynthesis, and induction of new tyrosine hydroxylase protein. These neurochemical changes occurred after sustained hypoxia only, suggesting that noradr energic neurons are involved in the central chemoreceptor pathway duri ng sustained hypoxia but are not essential for regulatory responses to acute hypoxia. Acute hypoxia elicited the expression of c-Fos protein in neurons located in nucleus tractus solitarius that were not catech olaminergic. Noradrenaline released under long-term hypoxia could play a neuromodulatory role in ventilatory acclimatization. Cardiovascular responses to hypoxia are mediated by changes in sympatho-adrenal outf low, different according to the target organ. Cardiac sympathetic outp ut and adrenal secretion were stimulated independently of carotid body chemoafferents. Early postnatal hypoxia induced long-term neurochemic al changes in carotid body, brainstem and sympathetic efferents that m ay reveal alterations in development of neurons involved in the chemor eceptor pathway. (C) 1997 Elsevier Science Inc.