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Immunocytochemical detection of serotonin content in raphe neurons of newborn and young adult rabbits before and after acute hypoxia
Author(s) -
Kim Chung S.,
McNamara M.Colleen,
Lauder Jean M.,
Lawson Edward E.
Publication year - 1994
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(94)90034-5
Subject(s) - hypoxia (environmental) , serotonergic , serotonin , dorsal raphe nucleus , endocrinology , medicine , raphe , apnea , intermittent hypoxia , fetus , biology , chemistry , oxygen , pregnancy , obstructive sleep apnea , genetics , receptor , organic chemistry
Abstract The present immunocytochemical study demonstrates serotonin (5‐HT) depletion in the dorsal raphe nucleus (DRN) of 3‐ and 21‐day‐old rabbits following exposure to mild (10% ambient partial pressure of oxygen) and severe hypoxia (5% ambient oxygen). Under the mild hypoxic condition, 5‐HT immunoreactivity in cells and fibers of the DRN was decreased in 3‐day‐old as well as 21‐day‐old rabbits, as indicated by decreased intensity of the staining compared to age‐matched controls. Although this decrease was more pronounced in the younger animals, recovery from mild hypoxia was seen in both age groups. Hypoxic effects were more striking in 3‐day‐old animals under the severe hypoxic condition, indicating a greater depletion of 5‐HT than in the mildly hypoxic condition. However, little additional effect on the older age group was seen. Further, a decreased ability of the 3‐day‐old rabbits to recover following severe hypoxia suggests that protracted effects on the developing serotonergic system occur following severe hypoxia during the neonatal period. This was demonstrated by the long‐lasting decrease in the number of stained cells and fibers of the DRN 4‐hr after return to normal conditions (21% O 2 ). We conclude that newborns have a decreased rate of 5‐HT synthesis and/or metabolic turnover that results in rapid depletion of intracellular stores and protracted time to recover from a hypoxic challenge. Similar effects could occur in human fetuses, newborns or infants following birth trauma, apnea or other events associated with severe hypoxia.