[The modulation of cerebral cortex and subcortical nuclei on NRM and their role in acupuncture analgesia].
The vast research have demonstrated that the acupuncture analgesia is effected through a physiological mechanism brought about by the nervous system, particularly the central nervous system. We combined the acupuncture effects and theory of channels and collaterals with the new advance of pain neurophysiology, and centred attention on nucleus raphe magnus (NRM), that is one of the origins of the important descending inhibitory pathways of the intrinsic analgesic systems in brain. The unit discharges of NRM neurons and their nociceptors/ph responses were recorded extracellularly with glass microelectrode at 1495 neurons on 634 wastar rats. The modulation of cerebral cortex, the head of N. caudatum (NCa), N. Accumbens (N. Ac), N lateral habenular (NHa) and Periaquaeductal gray matter (PAG) on NRM and their role in acupuncture analgesia were studied by central locational stimulation, lesion and microinjection. The result were as follows: 1. The most NRM neurons could respond to noxious stimulation of tail tip with increasing or decreasing firing rate. Electroacupuncture (EA) at "Zusanli" could activate the NRM neuron, increasing discharges, and inhibit their nociceptive responses, producing analgesia. 2. The activity of NRM neuron was modulated by PAG, NAc, and NCa. Stimulation at one of them can activate neuron of NRM, increasing firing rate, and induce analgesia. When the lesion or microinjection naloxone were made in PAG, NAc or NCa, EA analgesia could be weakened or lost, even the nociceptive responses might be increased. It is suggest that the nuclei participated in EA analgesia with their endogenous opiate like substance, and were playing an important role. It is also indicated that the electroacupuncture was used on the patients with some nuclei lesion or pathological changes should be careful to avoid making patients feel more painful. 3. Somatosensory area II (Sm II) of cerebral cortex participated in EA analgesia. The analgesic effects of EA at "Zusanli" were reduced after lesion of Sm II. The nociceptive responses could be inhibited by stimulation of Sm II. We have further demonstrated that analgesic effects of Sm II stimulation were achieved by the modulation of Sm II on NRM, via NAc and NHa closely related to limbic-midbrain system, and with NRM descending inhibitory pathways through dorsal lateral fasciculus (DLF) in the level of spinal cord. 4. The sensorimotor area (SM) of cerebral cortex seems was not necessary structure for EA analgesia. Either of hindlimb areas or larger range of bilateral SM were resected, the analgesic effects of EA at "Zusanli" were not obviously influenced. The stimulation of somatosensory area I (Sm I) of SM could inhibit the nociceptive responses of NRM neurons. It was also demonstrated the Sm I could modulate NRM by mediation of NCa of extrapyramidal system enhancing EA analgesia. Stimulation of Sm I could directly inhibit the nociceptive responses through pyramidal system in the level of spinal cord, producing analgesia. But the information of electroacupuncture was noxious stimulation, so it could be also inhibited by Sm I stimulation, playing an antagonism to EA analgesia. Thus when patient's emotion was very nervous or physical exercise was very strong, EA analgesic effects would be decreased. Therefore, in order to guarantee EA analgesic effects, it is necessary that patients should take a rest and calm down before electroacupuncture. The contrary action between pyramidal and extrapyramidal systems in EA analgesia may be the one of mechanisms of that EA analgesia to be not full and changeful.
Liu
X
X
Institute of Acupuncture and Moxibustion, China Academy of Traditional Chinese Medicine, Beijing.
D015667:Acupuncture Analgesia; D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology*; D015671:Electroacupuncture; D006801:Humans; D009619:Nociceptors / Q000502:physiology; D011903:Raphe Nuclei / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013003:Somatosensory Cortex / Q000502:physiology*