D Badillo-Martinez

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Neonatal administration of monosodium glutamate (MSG) destroyed perikarya in the arcuate nucleus and median eminence, including those that contain met-enkephalin and beta-endorphin and it increased the density of opiate receptors in the midbrain. Treatment with glutamate decreased the analgesic response on the jump test following a 10 mg/kg dose of(More)
Neonatal administration of monosodium glutamate (MSG) produces in rats 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(More)
Both opioid peptides such as beta-endorphin and met-enkephalin and nonopioid peptides such as vasopressin and oxytocin increase pain thresholds in rodents. Antisera raised against each of these peptides have been developed for use in immunocytochemical and radioimmunoassay procedures. The present study assessed whether central administration of antisera(More)
Neonatal administration of monosodium glutamate (MSG) results in a number of anatomical, physiological and behavioral abnormalities, including changes in pain thresholds and analgesic responses. The present study compared the onsets of MSG-induced changes in jump thresholds, hot-plate latencies, and body weight. At 30, 60 and 80 days of age, MSG-treated(More)
y-MSH POTENTIATES ACTH ANALGESIA. J.M. Walker* H. Akil, r .............. S.J. Watson* Mental Health Research Institute, University of| ~24 Po Michigan, Ann Arbor, MI 48109, USA I Fridoy Introduction: B-endorphin derives from a 31K dalton gly~oprotein termed pro-opiocortin. Other products of pro-opiocortin include one or more ACTH related peptides and a 16K(More)
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