Bruce Pomeranz

Naloxone blockade of acupuncture analgesia: endorphin implicated.

Abstract Electroacupuncture in awake mice produced analgesia to noxious heat stimuli causing a 54% increase in latency to squeak. Subcutaneous naloxone completely abolished this acupuncture analgesia implicating endorphin. Naloxone injections in control mice caused a 17% hyperalgesia suggesting that “normal” mice also release endorphin. These results imply that endorphin is released at a low basal rate in “normal” mice, and at a much higher rate during acupuncture.

Electroacupuncture analgesia could be mediated by at least two pain-relieving mechanisms; endorphin and non-endorphin systems

Abstract This present paper shows different levels of electroacupuncture analgesia (antinociceptive effect) induced by three different frequencies of stimulation (i.e. 0.2, 4 and 200 Hz); highest analgesia is induced at 200 Hz and lowest at 0.2 Hz. Naloxone (1 mg/kg) completely reverses the electroacupuncture effects at low frequency stimulation (4 Hz) but produces no inhibition at high frequency stimulation (200 Hz). Conversely, parachlorophenylalanine (320 mg/kg) partially blocks the high-frequency (200 Hz) analgesia but produces no effect on the low-frequency (4 Hz) electroacupuncture analgesia. This suggests that electroacupuncture analgesia induced by low frequency stimulation may be mediated by endorphins while high frequency stimulation is not endorphinergic but may be partly due to serotonin.

Suppression of noxious responses in single neurons of cat spinal cord by electroacupuncture and its reversal by the opiate antagonist naloxone.

Abstract Electroacupuncture reduced the electrophysiologic noxious responses of single cells in lamina V of cat spinal cord. Nonnoxious responses were unaffected. The suppression of nociception by electroacupuncture took 20 min to reach the peak and 20 min to wear off, delays which are similar to those in clinical and behavioral studies. To test the hypothesis that these delays were caused by a slow buildup of endorphins, naloxone was given intravenously and this blocked the electro-acupuncture effect. Additional evidence is reviewed which supports this endorphin-acupuncture hypothesis.

Monoaminergic mechanism of electroacupuncture analgesia

We studied the effects of systemic injections of monoamine depletors, enhancers or receptor blockers on electroacupuncture analgesia (EAA) in mice. The following results emerged. (i) EAA is reduced by depletors of monoamines (tetrabenazine, TBZ depletes all monoamines; para-chlorophenylalanine, PCPA depletes serotonin; alpha-methyl-para-tyrosine, AMPT depletes catecholamines). However, depletion of noradrenaline and increase of serotonin by disulfiram enhances EAA. (ii) Replacement of depleted monoamines after TBZ treatment by their precursors (5-HTP or L-DOPA) restores EAA. (iii) EAA is enhanced by potentiating serotonin and dopamine by probenecid. EAA is also enhanced by the administration of monoamine precursors (L-DOPA for dopamine, 5-HTP for serotonin). The dopamine receptor stimulator, apomorphine, reduces EAA. (iv) EAA is also reduced by receptor blockade of catecholamines (by haloperidol), or blockade of noradrenaline (by yohimbine) or serotonin (by cinanserin). However, blockade of dopamine by pimozide has no significant effect on EAA. There are two main conclusions: (i) EAA results are similar to those previously reported for SPA for all drugs except apomorphine and pimozide; and (ii) EAA shows consistent results only with manipulations of serotonin: the data indicating that EAA (at 200 Hz) is mediated by serotonin. Since previous studies show that raphe or DLF (dorsolateral fasciculus) lesions abolish EAA, we postulate that descending axons from raphe release serotonin to inhibit trigeminal or spinal cord nociception during EAA.

Scientific Bases of Acupuncture

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

Abstract Dextronaloxone, a recently synthesized stereoisomer, which was shown to possess much less opiate receptor affinity than levonaloxone, produces no reversal of electroacupuncture analgesia (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 mediated by opiate receptors. Possibly Type I receptors are the major component of this system.

Electroacupuncture Elevates Blood Cortisol Levels in Naive Horses; Sham Treatment has no Effect

It was hypothesized that electroacupuncture releases beta-endorphin and ACTH from the pituitary. Since ACTH induces the release of cortisol from the adrenal glands, blood cortisol level should be enhanced by electroacupuncture. The present result shows that the blood cortisol levels of horses are significantly increased after 30 min of electroacupuncture treatment while the sham treatment (control) shows an insignificant effect.

Sympathetic denervation impairs epidermal healing in cutaneous wounds

The involvement of peripheral nerves in dermal wound healing, particularly in the inflammatory response has not been extensively studied. Therefore, this study was performed to examine the role of peripheral nerves in the healing of rat skin linear incisions. We report that chemical sympathectomy with 6‐hydroxydopamine significantly impaired wound healing as measured on days 7, 11, and 14 postsurgery (by day 14, 48% of the sympathectomized rats were healed in contrast with 84% of the controls; p = 0.0104). In contrast, neonatal capsaicin treatment, which predominantly destroys sensory afferents, had no effect on wound healing (p > 0.05 on all days). These results support the hypothesis that sympathetic efferents are important for wound healing. Unlike previous research, which showed that peripheral nerves influence ischemic skin flaps, we are the first to demonstrate a role for peripheral nerves in the healing of skin incisions. Because inflammation is an important step in cutaneous wound healing, we propose that a reduction of neurogenic inflammation caused by sympathectomy may explain the impaired wound healing that we observed in our study.

Dexamethasone partially reduces and 2% saline-treatment abolished electroacupuncture analgesia: These findings implicate pituitary endorphins

Abstract Dexamethasone, a cortisol analogue which inhibits ACTH and endorphin release in a negative feedback system, partially reduces electroacupuncture analgesia (EAA) in mice. In addition, mice forced to drink 2% saline for 3 days (this reduces pituitary endorphin levels) had a complete loss of EAA. These two experiments support our previous finding that hypophysectomy abolishes EAA. Altogether, these results implicate pituitary endorphins in EAA.

Application of weak electric field to the hindpaw enhances sciatic motor nerve regeneration in the adult rat

Direct current (DC) electrical stimulation of the hindpaw is shown to enhance sciatic motor nerve regeneration in the adult rat. Cathodal stimulation, using weak currents (10 microA/cm2; field strength approximately 100 mV/cm) increased the reinnervation of the hindpaw muscles as measured by evoked electromyograms. This enhanced regeneration only occurred after cut-and-suture lesions, but not after crushing injury of the sciatic nerve. This enhancement of motor nerve regeneration by weak DC fields had been previously described in amphibians but we are the first to describe this phenomenon in mammals.