Impairments in Analgesic, Hypothermic, and Glucoprivic Stress Responses following Neonatal Monosodium Glutamate

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Abstract
Neonatal administration of monosodium glutamate (MSG) in rats produces neurotoxic degeneration of the circumventricular system, including the medial-basal hypothalamus, depleting several neuropeptides and neurotransmitters in this area. In addition, a number of behavioral and neuroendocrine responses are impaired, including a significant decrease in the analgesic response to cold-water swims (CWS). Whether the alterations in the analgesic responses following CWS and 2-deoxy-D-glucose (2-DG) induced by neonatal MSG treatment were due either to direct alterations in a pain-inhibitory system, or alternatively, to alterations in a system that processes the stressful consequences of properties of a stimulus. To accomplish this, the analgesic, hypothermic and locomotor responses following CWS and the analgesic, hyperphagic and locomotor responses following 2-DG were assessed in rats treated neonatally (days 2, 4, 6, 8 and 10) with either MSG or a vehicle solution. MSG-treated rats displayed significant reductions in both their analgesic and hypothermic responses following CWS, suggesting that MSG treatment impairs an animal''s ability to process sufficiently the stimulus properties of the swim as stressful. While MSG treatment potentiated 2-DG analgesia, it reduced 2-DG hyperphagia, suggesting that MSG treatment also impairs coping responses to glucoprivation. The importance of the circumventricular system in the coding of stimuli as potential stressors and in the subsequent activation of requisite systems necessary to provide a sustained, coordinated and synchronous coping response are indicated.