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Cerebrospinal fluid beta-endorphin in models of hyperalgesia in the rat. |
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AbstractCerebrospinal fluid (CSF) obtained by acute percutaneous puncture of the cisternal membrane of the halothane anesthetized rat has low but measurable concentrations of beta-endorphin-like immunoreactivity (beta-EPir: 32.8 +/- 3.0 pmol/l). Chromatographic separation of beta-EPir showed that authentic beta-endorphin1-31 was the main component of beta-EPir in cisternal CSF. Subcutaneous injection of 5% formalin in the hind paws did not increase beta-EPir in cisternal CSF. Rats with tactile paw hyperalgesia evoked by unilateral ligation of the L5/6 nerve roots 2 weeks earlier had beta-EPir concentrations that did not differ from sham operated or unoperated control animals. In contrast, capsaicin injected in the hindpaws increased the mean beta-EPir concentration compared to saline injections (P = 0.006) 45 min after emerging from anesthesia following injection. These results show that acute activation of C fibers (by capsaicin) will evoke the release of beta-endorphin into the CSF, suggesting activation of the beta-endorphin terminal systems in the brain/midbrain. The failure of formalin injections to release beta-EPir to CSF may be due to specificity of the afferent stimulus evoking beta-EPir release, a lower stimulus intensity, and/or the duration of the stimulus generated by formalin. The normal concentrations of beta-EPir found in the hyperalgesic state following nerve injury suggest that the supraspinal beta-endorphin system does not display tonic changes under such conditions.
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