Brain research
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When rats were tested more than two weeks following surgery, lesions of the medial basal hypothalamus centered on the arcuate nucleus enhanced a form of foot-shock stress-induced analgesia (SIA) that was not blocked by injections of the opiate receptor blocker, naltrexone (6 mg/kg;). These arcuate nucleus lesions reduced the SIA produced by the same stressor when similar rats were tested 3-4 days following surgery. ⋯ We suggest that arcuate nucleus lesions disrupt a system important for the elaboration of opiate-mediated SIA (Expt. 4), perhaps by damaging the brain's beta-endorphin system. In response to damage to this opioid analgesic system, we hypothesize that the damaged brain initiates time-dependent compensatory changes in an undamaged non-opioid analgesic system, resulting in enhanced non-opiate-mediated SIA.
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The effects of microinjection of 5-10 micrograms of morphine into the midbrain periaqueductal gray (PAG) on the activity of neurons in the rostral ventral medulla (RVM) were studied in lightly anesthetized rats. Based on the relationship between changes in neuronal activity and the occurrence of the tail-flick reflex (TF), RVM neurons were divided into 3 groups: off-cells, on-cells and neutral cells. The off-cells exhibited an abrupt pause and the on-cells an acceleration beginning just prior to the occurrence of the TF. ⋯ The effects on cell activity were reversed by systemically administered naloxone and were not seen following microinjections which failed to block the TF. Neutral cell activity was unchanged following microinjection of morphine into the PAG. These results support the hypothesis that off- and on-cells in the RVM mediate the effects of microinjection of morphine into the PAG on spinal nociceptive reflexes.
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The effects of sciatic nerve resection on lumbar dorsal root ganglion cells and their central branches have been studied in the adult rat. A quantitative analysis of the lumbar dorsal root ganglia indicated a 15-30% cell loss on the operated side. Argyrophilia indicating transganglionic degeneration was observed in Fink-Heimer stained sections from the lumbar spinal cord and the brainstem. ⋯ A few degenerating fibers could also be observed in the ipsilateral dorsal horn laminae V and VI, and in the ipsilateral ventral horn as well as in the contralateral dorsal horn and the gracile nucleus. The results confirm and extend previous findings at other levels and in other species. This suggests that cell loss and transganglionic degeneration may be general phenomena affecting a substantial proportion of primary sensory neurons following peripheral nerve injury.
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Modulation of the biphasic effect of muscimol on prolactin secretion by benzodiazepines and secobarbital was investigated, using an in vitro superfusion system. The stimulatory effect of low concentrations of muscimol was potentiated by both classes of drugs, and the effect of benzodiazepines appeared to be mediated by central-type benzodiazepine receptors. ⋯ Clonazepam reduced the potency of bicuculline methiodide as an antagonist of the stimulatory effect, but did not alter the potency of picrotoxinin. These results demonstrate a selective potentiation of one component of the GABAA receptor effect on lactotrophs by benzodiazepines and barbiturates and provide evidence for a functional effect of these drugs at a site without the CNS.
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Electrical stimulation of neurons located in the nucleus raphe magnus (NRM) produces antinociception which appears to result from inhibition of spinothalamic tract neurons located in the spinal cord dorsal horn. Iontophoretic application of acetylcholine also activates NRM neurons and microinjection of cholinergic agonists such as carbachol into the NRM produces a profound, long-lasting antinociception. Since the antinociception induced by electrical stimulation of NRM neurons is mediated, at least in part, by bulbospinal serotonergic and noradrenergic neurons, the role of these monoaminergic neurons in mediating the antinociception induced by microinjecting carbachol in the NRM was examined in the present study. ⋯ These results lead to the suggestion that the antinociception induced by the local injection of carbachol into the NRM is mediated by selective activation of bulbospinal noradrenergic neurons. Furthermore, the antinociception resulting from the activation of these descending noradrenergic neurons appears to be mediated by alpha 2-noradrenergic receptors located in the spinal cord dorsal horn. Finally, the local injection of carbachol into the NRM also appears to activate another population of noradrenergic neurons which produces hyperalgesia mediated by alpha 1-noradrenergic receptors.