We have known the endogenous opioid peptide beta-endorphin for 20 year
s. Surprisingly, our knowledge of the physiological role of this pepti
de and its receptors in modulation of pain perception is still fragmen
tary. Whereas most studies have tried to elucidate the physiological r
ole of beta-endorphin by reversing evoked responses by the opioid anta
gonist naloxone, this review focuses on quantification of release of b
eta-endorphin in the brain as the approach to define physiological and
pathophysiological roles of beta-endorphin in relation to nociception
. Using a lateral ventricle-cisterna magna perfusion model in the anes
thetized rat, it was shown that depolarization of neurons in the arcua
te nucleus of the hypothalamus, where beta-endorphin is produced, was
followed by release of beta-endorphin to the cerebrospinal fluid compa
rtment. Intense activation of spinal nociceptive pathways by intrathec
al capsaicin injections also led to beta-endorphin release. It is conc
luded that there may still be good reason to quantify beta-endorphin i
n human cerebrospinal fluid to elucidate the role of beta-endorphin in
pain perception. (C) Acta Anaesthesiologica Scandinavica 41 (1997).