Brain research
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Analgesia can be elicited following microinjections of morphine, mu-selective agonists and beta-endorphin into the amygdala. These analgesic responses are mediated by opioid synapses in the periaqueductal gray (PAG) since general (naltrexone), mu (beta-funaltrexamine) and delta2 (naltrindole isothiocyanate) opioid antagonists administered into the PAG significantly reduce both morphine and beta-endorphin analgesia elicited from the amygdala. Supraspinal multiplicative opiate analgesic interactions have been observed between the PAG and rostroventromedial medulla (RVM), the PAG and locus coeruleus (LC), and the RVM and LC. ⋯ Co-administration of beta-endorphin (1 microg) into the amygdala and morphine (1 microg) into the PAG produced a potent interaction, but co-administration of morphine (1 microg) into the amygdala and beta-endorphin (1 microg) into the PAG failed to produce interactive effects. Finally, co-administration of morphine (1 microg) and beta-endorphin (1 microg) into either the amygdala alone or the PAG alone failed to produce an interaction, indicating the importance of regional opioid activation. These data are discussed in terms of the test-specificity of nociceptive processing in the amygdala, in terms of the multiple modulatory mechanisms mediating beta-endorphin analgesia in the PAG, and in terms of whether the interactions are either mediated by anatomical connections between the amygdala and PAG or by mechanisms initiated by these two sites converging at another site or sites.
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The amygdala, periaqueductal gray (PAG), and rostral ventromedial medulla (RVM) are critical for the expression of some forms of stress-related changes in pain sensitivity. In barbiturate anesthetized rats, microinjection of agonists for the mu opioid receptor into the amygdala results in inhibition of the tail flick (TF) reflex evoked by radiant heat. We tested the idea that TF inhibition following opioid stimulation of the amygdala is expressed through a serial circuit which includes the PAG and RVM. ⋯ Since acute injection of lidocaine into the RVM also affected baseline heart rate, separate animals were prepared with small electrolytic lesions placed in the RVM. Chronic RVM lesions also blocked TF inhibition produced by amygdala stimulation but did not affect heart rate. These results, when taken together with similar findings in awake behaving animals, suggest that a neural circuit which includes the amygdala, PAG, and RVM is responsible for the expression of several forms of hypoalgesia in the rat.