Cerebrospinal fluid β-endorphin in models of hyperalgesia in the rat

Abstract

Cerebrospinal fluid (CSF) obtained by acute percutaneous puncture of the cisternal membrane of the halothane anesthetized rat has low but measurable concentrations of β-endorphin-like immunoreactivity (β-EPir: 32.8 ± 3.0 pmol/l). Chromatographic separation of β-EPir showed that authentic β-endorphin 1–31 was the main component of β-EPir in cisternal CSF. Subcutaneous injection of 5% formalin in the hind paws did not increase β-EPir in cisternal CSF. Rats with tactile paw hyperalgesia evoked by unilateral ligation of the L 5/6 nerve roots 2 weeks earlier had β-EPir concentrations that did not differ from sham operated or unoperated control animals. In contrast, capsaicin injected in the hindpaws increased the mean β-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 β-endorphin into the CSF, suggesting activation of the β-endorphin terminal systems in the brain/midbrain. The failure of formalin injections to release β-EPir to CSF may be due to specificity of the afferent stimulus evoking β-EPir release, a lower stimulus intensity, and/or the duration of the stimulus generated by formalin. The normal concentrations of β-EPir found in the hyperalgesic state following nerve injury suggest that the supraspinal β-endorphin system does not display tonic changes under such conditions.