Neonatal Monosodium Glutamate

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 β-lipotropin (β-LPH) and β-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 Iittermate controls, exhibited concomitant changes in the immunocytochemical distribution of ACTH and β-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-Z)-glucose, was unaffected by neonatal MSG treatment. Concomitant with these selective analgesic deficits, MSG-treated rats displayed a marked immunocytochemical reduction in ACTH/β-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.

Neurotoxic Lesions Induced by Monosodium Glutamate Result in Increased Adenopituitary Proopiomelanocortin Gene Expression and Decreased Corticosterone Clearance in Rats

“…As this was not the case, the suggestion of a higher content of POMC mRNA per corticotrope cell seems to be more probable. Accordingly, no difference in ACTH immunoreactivity in the pituitary was described in a previous study using a different experimental design [24]. …”

Mapping, in the rat central nervous system, of morphine‐induced changes in turnover of 5‐hydroxytryptamine.

“…A glance at the regions showing a large increase in 5-HT turnover after morphine (Table 2), shows that, also outside the cord, pain pathways are well represented; medulla, mid-brain and medial thalamus carry or respond to pain impulses, and the hypothalamus seems to be directly involved in certain stress-induced forms of analgesia, as well as in the analgesic response to morphine (Bodnar, Abrams, Zimmerman, Krieger, Nicholson & Kizer, 1980). In both hypothalamus and thalamus, electrical stimulation of regions near the midline causes analgesia (Rhodes & Liebeskind, 1978).…”