Brain research
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Exposure to an innocuous stimulus that has been paired with footshock during Pavlovian conditioning results in the activation of descending antinociceptive systems in the rat. Several recent studies indicate that the hypoalgesia observed when contextual stimuli are paired with shock and the formalin test is used to measure antinociception depends on the integrity of a neural circuit which includes the amygdala and the periaqueductal gray. The present experiment was designed to determine if the amygdala is also critical for hypoalgesia in response to a discrete auditory signal for footshock when hypoalgesia is measured with the radiant heat tail flick test. ⋯ After training, one half of the animals received large electrolytic lesions of the amygdala. Lesions of the amygdala blocked the time dependent elevation in tail flick latency following tone presentation in animals given paired training, but did not alter baseline tail flick responding. These data indicate that the amygdala is also essential for fear-related modulation of spinally mediated nociceptive reflexes, and provide further support for our current model in which amygdalo-mesencephalic projections are critical for the expression of certain forms of stress-induced hypoalgesia.
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In previous studies, we demonstrated that tyrosine hydroxylase and neurofilament proteins are regulated by chronic morphine and chronic cocaine treatments in the ventral tegmental area in Sprague-Dawley rats and that the inbred Lewis and Fischer 344 rat strains, under drug-naive conditions, show different levels of these proteins specifically in this brain region. In the current study, we compared Lewis and Fischer rats with respect to levels of adenylate cyclase, cyclic AMP-dependent protein kinase and G-proteins in the nucleus accumbens (NAc) and locus coeruleus (LC), brain regions in Sprague-Dawley rats where these proteins are regulated by chronic exposure to morphine or to cocaine. We found that levels of adenylate cyclase and cyclic AMP-dependent protein kinase activity are higher in the NAc and LC of Lewis rats compared to Fischer rats, whereas levels of Gi alpha and G beta were lower. ⋯ Moreover, Lewis and Fischer rats displayed very different opiate withdrawal syndromes, with different types of behaviors elicited upon precipitation of opiate withdrawal with the opiate receptor antagonist, naltrexone. The possible relationship between these behavioral findings and the biochemical and electrophysiological data is discussed. These studies provide further support for the possibility that Lewis and Fischer rat strains provide a useful model system in which some of the genetic factors that contribute to drug-related behaviors can be investigated.