Neonatal Monosodium Glutamate
Effects Upon Analgesic Responsivity and Immunocytochemical ACTH/β-LipotropinBodnar R.J. · Abrams G.M. · Zimmerman E.A. · Krieger. D.T. · Nicholson G. · Kizer J.S.
Department of Behavioral Physiology, New York State Psychiatric Institute; Departments of Neurology and Psychiatry, Columbia University College of Physicians and Surgeons, and Department of Medicine, Mt. Sinai School of Medicine, New York, N.Y., and Departments of Medicine and Pharmacology, University of North Carolina, Chapel Hill, N.C.
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.
© 1980 S. Karger AG, Basel
Dr. R Bodnar, Department of Behavioral Physiology, New York State Psychiatric Institute, 722 W. 168th Street, New York, NY 10032 (USA)
Received: July 27, 1979
Accepted after revision: October 3, 1979
Published online: March 26, 2008
Number of Print Pages : 5
Neuroendocrinology (International Journal for Basic and Clinical Studies on Neuroendocrine Relationships)
Vol. 30, No. 5, Year 1980 (Cover Date: 1980)
Journal Editor: Millar R.P. (Edinburgh)
ISSN: 0028–3835 (Print), eISSN: 1423–0194 (Online)
For additional information: http://www.karger.com/NEN