Please use this identifier to cite or link to this item:
|Title:||Mechanisms of Electroacupuncture Analgesia as Related to Endorphins and Monoamines: An Intricate System is Proposed|
|Authors:||Cheng, Shing Sou Richard|
|Abstract:||<p>It has been hypothesized (Cheng, M.Sc. thesis, 1977) that electroacupuncture analgesia (EAA) is mediated by endorphins, he endogenous morphina-like peptides. According to this previous hypothesis electroacupuncture (EA) stimulates the periaqueductal gray (PAG in the midbrain) to release enkephalins which will activate the raphe-DLF (dorsolateral faciculus) descending inhibitory system to block the pain messages (nociception) at the spinal cord level. In parallel, EA may stimulate the pituitary to release endorphins to produce analgesia. To further explore this hypothesis, several investigations were carried out on the mechanisms of EAA as related to endorphins and the monoamines (serotonin, dopamine and norepinephrine). EA experiments were carried out on B6AF1/J mice which were put in paper receptacles. Noxious responses to radiant heat were measured by the latencies to squeak. EA was applied by inserting stainless steel needles into the acupuncture point, HoKu (the first dorsal interosseus muscles). Drug injections (intraperitoneally) were done in a blind manner. Results suggest that EAA is mediated by stereospecific opiate receptors; the chief component may be the Type I opiate receptors (the latter are located mainly in the analgesic areas in the central nervous system and may be responsible for opiate analgesia). Evidence also demonstrated that EAA may involve pituitary endorphins and ACTH which are usually released together. Dexamethasone, a cortisone dertivative, suppressed EAA probably by a negative feedback inhibition of pituitary release. Two percent saline, which depresses pituitary endorphins also reduced the effectiveness of EAA. The ACTH released by EA causes elevated cortisol levels and a study shows that EA increases blood cortisol levels in horses. Several experiments (including one in this thesis) suggest that the D-amino acids (DAA), D-phenylalanine and D-leucine, produce analgesia by protecting endorphins from enzymatic degradation. The combined treatments with EA and DAA produced a higher analgesia in mice than either treatment alone. This suggests that EA may release endorphin which are protected by DAA, and hence, EA plus DAA together produce a higher analgesia. The present study also shows that EAA does not show cross-tolerance with morphine and that EA reduces signs of withdrawal in the morphine addicted mouse. In another experiment it was found that low frequency (4 Hz) EAA may be mediated by serotonin. Further EA experiments show that dopamine and norepinephrine modifying drugs do not give coherent results while those with serotonin manipulations are very consistent. By combining the results in this thesis with those in the literature I propose an intricate system for the mechanisms of EAA (Figure A). EA at 4 Hz may stimulate teh sensory afferent nerves to several brain regions. In the midbrain PAG, these stimuli release enkephalins which activate the raphe nuclei to send descending inhibition along the DLF to the spinal cord and block incoming pain messages. The DLF-descending inhibitory system may be partly mediated by the neurotransmitter, serotonin. In parallel, EA (4 Hz) may stimulate the beta-endorphin neurons in the hypothalamus and pituitary. The pituitary endorphins may be released into the blood circulation, or may backflow directly into the CSF (the endorphins in the circulation have to pass through the blood-brain barrier to bind to the opiate receptors in the brain for analgesia). If the acupuncture points and the painful areas are in the same segmental levels, EA (4 Hz) may also directly stimulate the release of endorphins in the spinal cord. High frequency (200 Hz) EAA may activate sensory nerves which directly stimulate the DLF-descending serotonin inhibitory systems, thus by-passing the PAG-endorphin systems. In summary, low frequency (4 Hz) EA may stimulate the release of endorphins in the spinal cord, midbrain, hypothalamus and pituitary for pain-relief, while high frequency (200 Hz) EA may directly stimulate the DLF-serotonin inhibitory systems, thus avoiding the endorphin links.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
Items in MacSphere are protected by copyright, with all rights reserved, unless otherwise indicated.