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  • Title: Effects of neonatal exposure to monosodium glutamate on the electrical activity of neurones in the mediobasal hypothalamus, and on the plasma concentrations of thyroid-stimulating hormone and prolactin, following stimulation of the rostral hypothalamus in adult female rats.
    Author: Saphier DJ, Dyer RG.
    Journal: J Endocrinol; 1981 Jun; 89(3):379-87. PubMed ID: 7252399.
    Abstract:
    Action potentials were recorded from 174 neurones in the mediobasal hypothalamus of ovariectomized adult female rats exposed neonatally to monosodium glutamate (MSG) and from 145 neurones in control rats. All of the animals, which were anaesthetized with urethane, had been ovariectomized for at least 3 weeks and received two injections of oestradiol benzoate (20 microgram/100 g body weight, i.m.) 72 h and immediately before the recording experiments. The response of each neurone to electrical stimulation of the median eminence and rostral hypothalamus (preoptic and anterior hypothalamus areas; PO/AH) was analysed. The most striking feature of the results obtained was the significant (P less than 0.001) loss of inhibitory responses in those neurones remaining in the adult rats after neonatal treatment with MSG. The loss of inhibitory responses applied to both stimulation sites. In each rat the response of one neurone, which was antidromically identified as projecting to the median eminence, was recorded before and during stimulation of the PO/AH at 50 Hz for 30s in every min for 15 min. Before and after this stimulation blood was collected from a jugular vein for estimation by radioimmunoassay of concentrations of prolactin and TSH. In the MSG-treated rats significantly (P less than 0.05) fewer neurones were inhibited by the 50 Hz stimulation than in control rats. In control rats the plasma concentrations of prolactin nearly quadrupled as an immediate consequence of this treatment, whereas in MSG-treated rats plasma concentrations barely doubled. However, in the MSG-treated rats plasma concentrations of prolactin continued to rise after stimulation ceased, possibly as a consequence of enhanced secretion of thyrotrophin releasing hormone.
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