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Long‐term influence of neonatal hypoxia on catecholamine activity in carotid bodies and brainstem cell groups of the rat.
Author(s) -
Soulier V,
Dalmaz Y,
Cottet-Emard J M,
Lagercrantz H,
Pequignot J M
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp021878
Subject(s) - hypoxia (environmental) , catecholaminergic , brainstem , endocrinology , catecholaminergic cell groups , carotid body , medicine , catecholamine , chemoreceptor , biology , dopamine , peripheral chemoreceptors , glomus cell , respiratory system , chemistry , oxygen , stimulation , receptor , organic chemistry
1. In order to determine the long‐term influence of neonatal hypoxia on catecholaminergic activity in peripheral arterial chemoreceptors and brainstem noradrenergic cell groups (A1, A2, A5 and A6), 1‐day‐old male rat pups were subjected to hypoxia (10% oxygen) for 6 days and then supplied with normal air. Control animals were kept at normoxia from birth. Rats were killed at either 3 or 8 weeks of age. 2. The content of dopamine and noradrenaline in carotid bodies of neonatally hypoxic rats was increased at both 3 and 8 weeks of age. 3. Noradrenaline turnover was selectively decreased in the caudal portion of A2 (located in the area of chemosensory afferent projection) at 8 weeks of age (‐76 +/‐ 2%), while this turnover was unaffected in rostral A2 cells. Noradrenergic activity in A1, A5 and A6 was altered by neonatal hypoxia in an age‐dependent fashion. 4. The data suggest that neonatal hypoxia induces long‐term changes in the basal activity of the carotid body and brainstem noradrenergic cell groups. Such changes might contribute to neuronal regulation of the delayed respiratory, arousal and neural sequelae associated with neonatal hypoxia. These changes could also be involved in the early programming of respiratory and blood pressure control.