Pain, 9 (1980) 385--390 © Elsevier/North-Holland Biomedical Press

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Abstracts

These abstracts have been selected and written by the Editorial Panel Leaders

PHYSIOLOGY

Suppression Of nociceptive responses in the primate by electrical stimulation of the brain or morphine administration: behavioral and electrophysiological comparisons. -- R.L. Hayes, D.D. Price, M. Ruda and R. Dubner, Brain Res., 167 (1979) 417--421.

The behavioral responses and the response of spinothalamic tract neurons to noxious stimulation were examined m monkeys both with electrical stimulation of a site in the central gray matter of the midbrain and with mor- phine given intravenously. The electrical stimulation of a strictly circum- scribed site in the midbrain caused prolonged suppression of spinothalvx~ic neurons in laminae I, IV and V. The same suppression occurred with mor- phine. Naloxone reversed the morphine suppression but not the suppression caused by midbmin stimulation. Both midbrain stimulation and morphine suppressed" the responses of awake monkeys to noxious thermal stimulation of the lip and the tail.

PHARMACOLOGY

Rapid changes in enkephalin levels in rat striatmn and hypothalamus induced by d iazepam. - T. Duka, M. Wuster and A. Herz, Naunyn-C;chmiedeberg's Arch. exp. Path. Pharrnak., 309 (1979) 1--5.

Benz0diazepines, widely used thempeutica!ly as minor trmlquilizers, have been shown to affect the action of many putative neurotmnsmitters. Whereas recent reports indicate a predominant effect of benzodiazepines on 7-aminobutyric acid, other studies have demonstrated modulatory influences of benzodiazepines on the content and/or turnover rate of acetylcholine, catecholamines and 5-hydroxytryptamine.

The acute treatment of rats with diazepam induces pronounced changes in brain enkephalin concentrations, as was estimated for methionine (met)- enkephalin and in some representative experiments for leucine (leu)-enke- phalin, employing highly specific radioimmunoassays. Diazepam selectively increased the enkephalin concentrations in the hypothalamus by about 35%, and lowered it in the corpus striatum by roughly 25%; no changes could be detected in the medulla oblongata/pons or m~dbrain. The drug-induced changes displayed a rapid onset. Peak effects were reached by 2--5 rain -after injection. Changes observed in the hypothalamus were only short lasting and were apparently par~dleled by diazepam concentrations in the brain, whereas

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the decrease in the striatum was of markedly longer duration. Presently, the mechanism underlying all these changes is unknown. Whereas an increase in enkephalin concentrations in the hypothalamus may be discussed in terms of the anti-stress effect of benzodiazepines, the observed drop in striatal enkephalin is not obviously to be correlated to behavioral changes induced by these drugs.

Autoanalgesia: acquisition, blockade and relationship to opiate b ind ing . - W.T. Chance, A.C. White, G.M. Krynock and J.A. Rosecrans, Europ. J. Pharmacol., 53 (1979) 461--468.

Acquisition of autoanalgesia (behaviorally activated antinociception) was assessed across 7 consecutive days by shocking rats 10 sec after the deter- ruination of their tail-flick latencies. Thus the effect of conditioned fear on antinociception was being investigated, since each shock preceded the subse- quent tail-flick test by 24 h. Autoanalgesia was acquired by the second fear- conditioning trial. Although pretreatment with naltrexone or diazepam had no effect, spinal cord transection at the thoracic level effectively obviated autoanalgesia. Investigations of opiate and opioid binding indicated signifi- cantly less binding in the fear-conditioned rats as well as in inverse relation- ship between binding and antinociception. These changes in binding are suggestive of partial mediation of autoanalgesia by an endogenous opiate peptide that is released by the fear-conditioning procedure.

Electroacupuncture analgesia is mediated by stereospecific opiate receptors and is reversed by antagonists of type 1 receptors . - R.S.S. Cheng and B.H. Pomeranz, Life Sci., 26 (1980) 631--638.

Recent results suggest that acupuncture analgesia (antinociceptive response) is mediated by the binding of endorphins to opiate receptors. The best evidence is that naloxone (an opiate an~gonist) inhibits the following processes: (a) electroacupuncture-mediated reduction of noxious responses of neurons in cat spinal cord, (b) electroacupuncture analgesia (EAA) in mice. and (c) analgesia induced in humans by acupuncture or transcutane- ous stimulation.

Dextronaloxone, a recently synthesized stereoisomer, which was shown to possess much less opiate receptor affinity than levor:aloxone, produces no reversal of EAA in mice. Since levonaloxone completely reverses EAA, this proves that stereospecific opiate receptors are involved. It has been reported that there are two classes of opiate receptors: type I and type II. Type I opiate receptors may be responsible for opiate analgesia. Antagonists of type I receptors, levonaloxone, naltrexone, cyclazocine and diprenorphine, all block electroacupuncture analgesia at low doses. All together, these results strongly support the hypothesis that electroacupuncture analgesia is medi- ated by opiate receptors. Possibly type I receptors are the major component of this system.