Monosodium glutamate neurotoxicity: a sex-specific impairment of blood pressure but not vasopressin in developing rats.
Neonatal administration of monosodium glutamate (MSG) results in severe adenohypophyseal endocrine malfunction as a result of hypothalamic neurotoxic lesioning. The present study examined the effects of administration of MSG on the neurohypophyseal vasopressinergic (AVP) system and systolic blood pressure (SBP) in adulthood. Monosodium glutamate or hypertonic sodium chloride was administered to male and female rat pups on days 1, 3, 5, 7 and 9 after birth. MSG treatment produced several features characteristic of the MSG-toxicity syndrome, including obesity, anterior pituitary dysgenesis and hypogonadism. However, MSG did not alter neurohypophyseal AVP profiles: AVP content of the posterior pituitary and microdissected regions of the hypothalamus and brainstem were similar in MSG-treated and control rats. Furthermore, MSG treatment did not alter water intake, serum AVP concentration, or the ability to reduce urine output in response to water deprivation. Thus, despite insult to adenohypophyseal function by neonatal administration of MSG, the neurohypophyseal AVP system remained functionally intact. In contrast, neonatal treatment with MSG altered SBP in a sex dependent manner. Female MSG-treated rats, unlike male MSG-treated rats, exhibited consistent systolic hypotension when compared with the NaCl-treated or non-treated control rats at 6, 9 and 12 weeks of age. Despite this chronic hypotension in MSG-treated female rats, heart rate was not altered and serum AVP was not elevated. These observations suggest a resetting of the baroreflex, attributable to neonatal administration of MSG.