PubMed · 14478282
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M NAMIKI, K TUNEMATSU, H SANO, T SAKANO, T YAMATERA, S ISHIDA. 1962. [TF administration before gastroscopy].. https://pubmed.ncbi.nlm.nih.gov/14478282/
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The distribution of delta-opioid receptors (DORs) in the rat central nervous system has been previously characterized by radioligand binding and immunohistochemistry. However, the functional neuroanatomy of DORs has not been mapped in any detail; this is potentially important, because these receptors appear to be primarily cytosolic. Opioid receptors can couple to G(i/o) G proteins, a process that is detected by agonist-stimulated [35S]guanylyl-5'-O-(gamma-thio)-triphosphate ([35S]GTPgammaS) binding. The purpose of this study was therefore to determine the distribution of functional DORs, as assessed by [35S]GTPgammaS autoradiographic labeling in response to the DOR agonist deltorphin II. For comparison, adjacent sections were labeled with [125I]deltorphin II or the DOR antagonist [125I]AR-M100613. In all three assays, mu-opioid receptors were blocked pharmacologically. The distributions of [125I]deltorphin II and [125I]AR-M100613 were highly correlated but not identical. Deltorphin II increased [35S]GTPgammaS binding in a concentration-dependent and naltrindole-sensitive manner. The regional [35S]GTPgammaS response to deltorphin II was only moderately predicted by agonist or antagonist radioligand binding (r = 0.67 and 0.50, respectively). [35S]GTPgammaS responses to deltorphin II were strongest in the extended striatum (caudate putamen, nucleus accumbens, olfactory tubercle) and cerebral cortex. In contrast, some areas reported to mediate DOR analgesia (brainstem, spinal cord) possessed a much lower [35S]GTPgammaS response. These findings demonstrate the existence of a partial mismatch between DOR radioligand binding and [35S]GTPgammaS response. This divergence possibly reflects regional heterogeneity in G-protein receptor coupling, or in the subcellular localization of DOR.
Evidence indicates that genetic, gender, and emotional/attentional aspects modulate the pain sensation. The present study examined the effect of swim-stress on nociceptive responses in Lewis (LEW) and spontaneously hypertensive (SHR) inbred rats (contrasting for anxiety-related behaviors), as well as in Wistar (WIS) rats of both sexes. Furthermore, we explored possible neurochemical mechanisms involved. In addition, we investigated whether habituation in the hot-plate apparatus could modify the hypoalgesic phenotype of SHR. Male and female LEW, SHR, and WIS rats were tested immediately before and 2 min after a 3-min swim in 15 degrees C water. The swim-stress induced analgesia in LEW and WIS, but not in SHR male rats. The same stressor induced analgesia in females of all three strains. In WIS female rats, the stress-induced analgesia (SIA) seems to involve, at least partially, a nonopioid N-methyl-d-aspartate (NMDA) analgesic system. Moreover, five brief exposures (90 s; 10-min intertrial interval) to the unheated hot-plate apparatus completely abolished the differences in basal hot-plate latencies observed in SHR compared with LEW and WIS strains. The present results demonstrate genetic and gender differences in nociceptive sensitivity and in the activation of endogenous analgesic systems in rats and highlight the influence of emotional reactivity. The SHR's hypoalgesic phenotype seems to involve central cognitive processes. Therefore, the LEW and SHR inbred strains may provide an important tool for study of the molecular bases underlying nociception and its modulation and the relationship with emotional/attentional processes.
Transmission of pain signals evoked by tissue damage leads to sensitization of the peripheral and central pain pathways. Pre-emptive analgesia is a treatment that is initiated before the surgical procedure in order to reduce this sensitization. Owing to this 'protective' effect on the nociceptive system, pre-emptive analgesia has the potential to be more effective than a similar analgesic treatment initiated after surgery. Theoretically, immediate postoperative pain may be reduced and the development of chronic pain may be prevented. Although some clinical studies have demonstrated significant effects on acute postoperative pain, no major clinical benefits of pre-emptive analgesia have been documented. The only way to prevent sensitization of the nociceptive system might be to block completely any pain signal originating from the surgical wound from the time of incision until final wound healing. Other pharmacological interventions, including 'antihyperalgesic' drugs such as NMDA-receptor antagonists and gabapentin, may interfere with the induction and maintenance of sensitization. Future studies will investigate the analgesic effect of prolonged multimodal combinations of different classes of 'traditional' analgesics and 'antihyperalgesics' on postoperative pain.