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  • Title: Neonatal monosodium glutamate. Effects upon analgesic responsivity and immunocytochemical ACTH/beta-lipotropin.
    Author: Bodnar RJ, Abrams GM, Zimmerman EA, Krieger DT, Nicholson G, Kizer JS.
    Journal: Neuroendocrinology; 1980 May; 30(5):280-4. PubMed ID: 6247667.
    Abstract:
    Neonatal administration of monosodium glutamate (MSG) produces neurotoxic degeneration of the retina and medial-basal hypothalamus, including the arcuate nucleus. Since this hypothalamic area contains the only neuronal cell bodies in brain which contain adrenocorticotrophic hormone (ACTH) and beta-lipotropin (beta-LPH) and beta-endorphin, destruction of these cells by MSG may interfere with pain responses mediated by nerve fibers arising from these perikarya. The present study examined whether MSG-treated rats, as compared to littermate controls, exhibited concomitant changes in the immunocytochemical distribution of ACTH and beta-LPH, and their reactivity to several analgesia-inducing manipulations. Although MSG-treated rats did not differ from control rats in their baseline reactivity to electric shock, they displayed an inability to exhibit analgesia following acute exposure to cold-water swim stress. In addition, MSG-treated rats showed an attenuated analgesic response following morphine administration. However, the analgesia elicited by either abrupt food deprivation, or the glucoprivic stress of 2-deoxy-D-glucose, was unaffected by neonatal MSG treatment. Concomitant with these selective analgesic deficits, MSG-treated rats displayed a marked immunocytochemical reduction in ACTH/beta-LPH perikarya and terminals in brain, but not pituitary. These data indicate that multiple pain-inhibitory systems exist, and that some rely upon an intact medial-basal hypothalamus to produce analgesia.
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