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386 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 binding.- 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.

Electroacupuncture analgesia is mediated by stereospecific opiate receptors and is reversed by antagonists of type 1 receptors

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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.