AP and Neurology
APA AND NEUROLOGY (3/4)
Lou_Z; Sun W; Liu Y; Tong Z (1992) [Effect of EAP on cortical and hippocampal EEG in adjuvant arthritis rats]. Chen Tzu Yen Chiu 17(2):129-132. Dept of Physiolgy, First Military Med Univ, Guangzhou. Adjuvant arthritis (AA) rats were used as the chronic pain model. Cortical and hippocampal (HPC) EEGs were recorded. Behaviour and local inflammatory reaction were observed. Desynchronization of the ECoG and HPC EEG in the AA rats induced an arousal response; beta waves increased and delta waves decreased significantly. However, the effect of desynchronization was inhibited by EAP on bilateral ST36 points and morphine. The cortex and hippocampus participate in the modulating action of chronic pain, and EAP has an analgesic action.
Lu_Z; Cao W; Dong X; Deng Y; Zhang T (1990) [Relation of capsaicin-sensitive neurones to the effect of EAP analgesia]. Chen Tzu Yen Chiu 15(3):213-216. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. Rats treated with capsaicin (50 mg/kg) sc on d 2 of life were used 12 wk after injection. The levels of Substance-P (SP) in sciatic nerves and dorsal spinal cords were measured with RIA to evaluate the extent of C-afferent fibres damaged by capsaicin. Results: Mean levels of SP in the sciatic nerve and dorsal spinal cord were decreased by 69 and 62% respectively, suggesting massive degeneration of the primary C-afferent fibres. Compared with controls, mean basal tail-flick latency (on immersion in 50oC water) was prolonged 105%. After EAP, mean tail-flick latency of capsaicin-treated rats was increased by 81%, while that of the vehicle-treated rats increased by 54%. C-afferent fibres substantially mediate transmission of noxious thermal stimuli, but are not essential for the transmission of AP-signals to induce APA.
Luo_M; Wang P; Yang Y (1991) [Effect of APA on synapses of paraventricular nucleus observed with transmission electron microscope]. Chen Tzu Yen Chiu 16(2):100-102. Inst of AP, China Acad of TCM, Beijing, PRC. In order to study the ultrastructural change of the paraventricular nucleus of hypothalamus during EAP, 13 healthy and adult rats were assigned to 2 groups: 1=Control (untreated) and; 2=EAP-treated. Paraventricular nucleus synapses belong mainly to the axodendricular asymmetrical synapses and contain many clear synaptic vesicles. Compared with the control, EAP very significantly (p <.01) decreased the number of vesicles. The paraventricular nucleus is involved in the EAP analgesia.
Mo_Q; Gong B; Fang J; Li J; Huang J; Chen K; Kuang X; Wang J (1994) [Influence of AP at ST36 on function of 5-HT and muscarine (M) receptor in rat's brain and spleen]. Chen Tzu Yen Chiu - AP Research 19(1):33-36. Shanghai Univ of TCM, PRC. Three groups of rats were studied: groups needled at ST36 (test group), or LV03, or not needled (control groups). Using receptor radioligand binding assay (RLBA), 5-HT and M receptors total binding capacities (Rt) were determined in different brain areas and spleen after needling. Compared with the control group, needling at ST36 gave clear APA and significantly decreased 5-HT and M receptors Rt in the cerebral cortex, hippocampus, striatum, spinal cord and spleen. 5-HT Rt was obviously decreased in brain stem and medulla oblongata but not in the thalamus. M receptor Rt value fell significantly in the thalamus but not in the brain stem and medulla oblongata. Different AP points had different effects on various Channels; AP at ST36 gave results different from those of LV03.
Moret_V; Forster A; Laverriere MC; Lambert H; Gaillard RC; Bourgeois P; Haynal A; Gemperle M; Buchser E (1991) Mechanism of analgesia induced by hypnosis and AP: is there a difference?. Pain May 45(2):135-140. Dept of Anaesthesiol, Hospital Cantonal Univ of Geneva, Switzerland. Hypnosis and AP can alleviate experimentally induced pain but the mechanism of analgesia remains unclear for both techniques. Experimental pain was induced by cold pressor test (CPT) in 8 male volunteers. Analgesic effect of hypnosis (HA) and AP (AA) was assessed before and after double-blind administration of placebo or naloxone, in a prospective, cross-over study. Pain intensity was significantly lower with HA as compared with AA, both with naloxone (p <.001) and placebo (p <.001). Within HA or AA groups, pain scores did not differ significantly when naloxone or placebo was administered. During AA, however, pain scores were similar to control values when naloxone was given (p=.05) but decreased significantly with placebo (p <.002). Analog scales for pain intensity and pain relief showed a good correlation (r=.94). Plasma levels of beta-End did not change significantly in any combination. Heart rate, peripheral arterial blood pressure and skin conductance were very insensitive indices to assess pain intensity or relief, as well as intensity of AP stimulation or depth of hypnotic trance. Conclusions: 1. HA and AA can significantly reduce pain from Cold Pressor Test, and HA is more effective than AA; 2. HA and AA are not primarily mediated by the opiate endorphin system; and 3. Plasma levels of beta-End are not significantly affected by either HA or AA nor by naloxone or placebo administration.
Nezhentsev_MV; Aleksandrov SI (1991) [The effect of psychotropic agents on the efficacy of AP reflexotherapy]. Vrach Delo Sep 9:19-24.
Omana_I; Olvera V; Santos P; Calderon JL (1994) Naloxone prevents reduction of pain responses evoked by AP in neuropathic rats. Proc West Pharmacol Soc 37:135-136. Dept Neurophysiol, Inst Mexicano de Psiquiatria, Mexico.
Pain_YZ; Wang LH; Tang YH; Yin XM; Wang S (1992) Reversal by gallamine triethiodide of the antagonistic effect of Ca2+ injection into habenula on EAP-analgesia. Sheng-Li-Hsueh-Pao Aug 44(4):326-332. Dept of Physiology, Norman Bethune Univ of Med Sci, Changchun. Bilateral intracranial cannulae were used for ic injection of 1 mol/L CaCl2 0.5 uL, 0.06 mol/L ACh 0.5 uL, 5.4 x 10-3 mol/L gallamine triethiodide (cholinergic nicotinic receptor blocker) 0.5 uL and 14.4 x 10-3 mol/L atropine (cholinergic muscarinic receptor blocker) 0.5 uL in the habenula of rats. Pain threshold before and after ic injection was measured by the latency of the tail-flick reflex, elicited by exposure to radiant heat. CaCl2 significantly reduced the basic pain threshold and weakened the effect of AP-analgesia (APA). ACh antagonized the effect of APA. Gallamine triethiodide raised the pain threshold almost to the raised level attained by APA; atropine only weakly and briefly strengthened the APA-effect on pain threshold. The antagonistic effect of Ca2+ on APA may be mediated via ACh in habenula.
Raevskaia_OS (1992) Nociceptive sensitivity of rabbits in varying localization of pain stimuli and naloxone administration. Patol Fiziol Eksp Ter Sep-Dec(5-6):7-9. Study of the dynamics of changes of evoked potential (EP) amplitude in electrodental and electrocutaneous stimulation (EDS and ECS, respectively) as an index of the perceptual component of the nociceptive reaction showed that 0.2 mg/kg and 0.5 mg/kg doses of naloxone produce both a hyper- and an analgesic effect in rabbits. The effect of naloxone depended on the individual properties of the rabbits, while its degree was determined by the localization of the nociceptive stimulus. The animals' individual properties were manifested by the presence or absence of an analgesic effect of Ear-EAP-sensitive (ES) or EAP-resistant (ER) rabbits. Naloxone injection caused a dose-dependent hyperalgesic effect in AS animals and an analgesic effect in ER rabbits in EDS. Similar effects were recorded in ECS, but their degree differed: hyperalgesia in ES rabbits occurred more clearly than analgesia in ER animals.
Rogvi-Hansen_B; Bach FW (1990) [APA: Neurochemical and neurophysiologic aspects]. Ugeskr Laeger Dec 152(49):3684-3687. Rigshospitalet, Kobenhavn, neuromedicinsk afdeling. AP has been used as an analgesic method for millenia without its mechanism of action being understood. In the past 2 decades, evidence has accumulated that AP activates an intrinsic neural network which monitors and modifies the activity of pain-transmitting neurons. Pain-suppression is partly mediated by endogenous opioid peptides and monoamines. The pain-inhibition system is organized at 3 levels of the neuroaxis: spinal cord, medulla and the midbrain. The raphe magnus nucleus and the spinal cord constitute a fundamental circuit while the PAG funnels the influences from the more rostral structures and collects signals from the spinal cord. PAG initiates descending and ascending inhibition resulting in pain reduction. The endogenous pain-control system may be elicited by other physiological stimuli and the effect of AP is unlikely to be specific.
Sato_T; Takeshige C; Shimizu S (1991) Morphine analgesia mediated by activation of the AP-analgesia-producing system. AETRIJ 16(1-2):13-26. Dept of Physiol, Sch of Med, Showa Univ, Tokyo, Japan. Analgesia caused by 0.5 mg/kg morphine ip (MA) in rats is equivalent to APA caused by low frequency stimulation of the tibial muscle (ST36). Analgesia equivalent to both APA and MA was produced by i.t. application of 0.05 ug morphine. This analgesia shows individual variation in effectiveness which is parallel to those of both APA and MA, and disappears after 250 mg DPA/kg ip. Analgesia that persisted after termination of AP stimulation was not affected, maximally developed MA and APA were both partially antagonized, and the initial development of APA and MA were completely antagonized by i.t. application of 0.2 ug naloxone. Analgesia caused by i.t. 0.05 ug morphine was abolished by bilateral lesion of the anterolateral tract (ALT) of the spinal cord and that caused by AP stimulation was abolished by contra-lateral lesion. Analgesia caused by larger doses (0.1-0.2 ug) of i.t. morphine was not abolished, but persisted after ALT lesion, unilateral lesion of the dorsal periaqueductal central grey (D-PAG), or hypophysectomy. Potentials were evoked by AP stimulation in the bilateral D-PAG. Analgesia produced by D-PAG stimulation was not affected by ALT lesion nor by i.t. naloxone, but was abolished by lesion of the dorsolateral funiculus. These results imply 2 types of morphine action in the spinal cord to produce analgesia: activation of the ascending APA pathway; and direct inhibition of pain message in the spinal cord. They also show that the APA producing pathway ascends contralaterally in the ALT and then bilaterally in the D-PAG.
Scherder_EJ; Bouma A (1993) Possible role of the nucleus raphe dorsalis in analgesia by peripheral stimulation: theoretical considerations. AETRIJ Jul-Dec 18(3-4):195-205. Inst of Physiotherapy and AP, Free Univ, Amsterdam, The Netherlands. Direct stimulation of the Nucleus Raphe Dorsalis (NRD) is very effective for obtaining analgesia. However, the possible role of the NRD in analgesia by peripheral stimulation, e.g. EAP or TENS, has received less attention. Most studies show that in particular the nucleus reticularis gigantocellularis, the nucleus raphe magnus, the nucleus reticularis magnocellularis, the locus coeruleus, and the PAG may participate in the supraspinal mechanism for the antinociceptive effect of peripheral stimulation. This paper presents theoretical considerations of the role of the NRD in analgesia by peripheral stimulation. Little direct evidence suggests that the NRD-serotonergic system might contribute to this type of analgesia. The analgesic role of specifically the serotonergic neurons of the NRD in peripheral stimulation was supported by indirect evidence. From studies of direct stimulation of the NRD, two other mechanisms by which peripheral stimulation might exert antinociceptive effects through the NRD have been hypothesized. Stimulation-parameters affecting the effectiveness of peripheral NRD stimulation will be discussed.
Shatskaia_NN; Komleva LM; Tarasova LA (1992) [Role of neuropeptides in the pathogenesis of pain syndrome in autonomic and sensory polyneuropathy of occupational etiology and their role in the therapeutic action of laser-AP]. Gig Tr Prof Zabol (1):25-27. Biochemical studies of opiate system in patients with occupational diseases showed the role of the central pain regulating system inducing the pain syndrome in autonomic and sensory polyneuropathy caused by occupational factors. Increased production of the pain-reducing endogenic neuropeptides such as endorphin and Leu-Enk was one of the means by which He-Ne laser-AP restores human adaptation to pain. A repeated course of laser-AP therapy would normalize the level of both neuropeptides. Blood levels of neuropeptides may serve to evaluate pain syndromes and estimate effects of laser-AP therapy.
Shen_X; Zhang W; Yu W (1993) [The influences of AP on the cortical evoked potentials in rabbits]. Chen Tzu Yen Chiu 18(1):24-28. Shanghai Coll of TCM, PRC. The effects of AP on visual, auditory, somatosensory evoked cortical potentials as well as raw EEGs were observed in 31 rabbits either anaesthetized with urethane or conscious. Results: 1. AP significantly depressed the main components of the evoked potentials; 2. AP desynchronized raw EEGs, while the animals appeared to be slightly activated; 3. AP decreased both the integral values of raw EEGs and the powers of lower frequency waves (1-3.99 Hz); these positively correlated well with the amplitudes of the main components of the evoked potentials. Conclusion: The effects of AP on evoked potentials may be secondary to the changes of EEGs; the inhibition of evoked potentials during AP does not necessarily mean that the cerebral cortex is inhibited.
Shu_J; Li KY; Huang DK (1994) The central effect of EAP analgesia on visceral pain of rats: a study using the [3H] 2-deoxyglucose method. AETRIJ Jun-Sep 19(2-3):107-117. Dept of Neurobiol, Shanghai Med Univ, PRC. This study had the objective to understand the central effect of EAP analgesia (EAA) on visceral pain of rats. We used the method of Sokoloff's 2-deoxyglucose (2-DG) auto-radiographic quantitative analysis to observe the changes of local cerebral metabolic rate of glucose (LCMRG) in rats given electrostimulation of greater splanchnic nerve (GSN) followed by EAP. The LCMRG had a significant difference between EAA group and pain group at some structures, such as the spinal thoracic and lumbar dorsal horns (segments T6-T8, L1-L3), locus coeruleus (lc), nucleus raphe magnus (rm), nucleus reticular gigantocellularis (rgi), periaqueductal grey (PAG) and habenulae lateralis (hl) of the thalamus. The results, combined with reports by other workers, suggest that these local cerebral structures may be the key nuclei in EAP-analgesia on visceral pain.
Shu_J; Li KY; Huang DK (1994) The central effect of EAP-analgesia on visceral pain of rats: a study using the 3H-2-deoxyglucose method. AETRIJ Jun-Sep 19(2-3):107-117. Dept of Neurobiology, Shanghai Med Univ, PRC. This study had the objective to understand the effect of EAP-analgesia (EAA) in the CNS on visceral pain of rats. We used the method of Sokoloff's 2-deoxyglucose (2-DG) auto-radiographic quantitative analysis to observe changes of local cerebral metabolic rate of glucose (LCMRG) in rats given electrostimulation of greater splanchnic nerve (GSN) after EAP. LCMRG was significantly different between EAA group and pain group at some structures, such as the spinal thoracic and lumbar dorsal horns (segments T6-T8, L1-L3), locus coeruleus (lc), nucleus raphe magnus (rm), nucleus reticular gigantocellularis (rgi), PAG and thalamic habenulae lateralis (hl). These local cerebral structures may be the key nuclei in the mechanism of EAA on visceral pain.
Simmons_MS; Oleson TD (1993) Ear-electrical stimulation and dental pain threshold. Anaesth Prog 40(1):14-19. Dept of Orofacial Pain and Occlusion, UCLA Sch of Dentistry. A modified double-blind study of naloxone reversibility of dental EAP-analgesia produced by Ear-Electrostimulation (EES) was examined in 40 subjects assigned at random to 4 groups: ES=EES followed by saline; EN=EES followed by naloxone; PS=Placebo EES followed by saline and; PN=Placebo EES followed by naloxone. Dental pain threshold was tested using a hand-held dental pulp tester. A second investigator used an electrostimulator to give the true or placebo EES. A third investigator injected saline or naloxone iv. The subjects and investigators 1 and 3 were blind to all treatment conditions. A repeated measures analysis of variance showed a significant difference among the 4 groups. EES gave a statistically significant 18% elevation of pain threshold, whereas PS and PN (placebos) remained essentially unchanged. ES increased mean pain threshold to >23% but EN (naloxone) decreased pain threshold to <12%. A small but significant elevation of pain threshold by EES is partially blocked by naloxone. An endogenous opioid system is one mechanism for EAP-analgesia.
Song_CY1; Liu WY; Gu XY; Lin BC (1993) Effect of anti-opioid peptide sera on oxytocin-induced enhancement of EAP-analgesia (EAA). Sheng Li Hsueh Pao Jun 45(3):231-236. Dept of Neurobiology, Second Military Med Univ, Shanghai, PRC. Effects of icv injection of anti-opioid peptide sera on oxytocin-induced enhancement of EAA were observed in this study. Injection of anti-beta-End serum (AEPS) alone attenuated EAA in rats. Injection of AEPS before icv injection of oxytocin did not block the enhancement of EAA by oxytocin. The antidynorphin A1-13 serum (FROMYNS) alone also reduced EAA, whereas injection of FROMYNS before injection of oxytocin potentiated the enhancement of EAA by oxytocin. However, neither anti-Met-Enk serum nor anti-Leu-Enk had any effect on the enhancement of EAA by oxytocin. EAA was attenuated by dynorphin but enhanced by oxytocin, but Beta-End and enkephalin did not affect this role of oxytocin. Enhancement of EAA by oxytocin is not dependent upon the endogenous opioid peptides in brain.
Takakura_N1; Kanamaru A; Sibuya M; Homma I (1992) Effect of AP at right LI04 point on the bilateral vibration-induced finger flexion reflex in man. AJCM 20(2):115-126. Japan Central AP and Moxibustion Coll, Tokyo, Japan. Vibration applied to the volar side of the finger tip induces a finger flexion reflex. AP is reported to inhibit this vibration-induced finger flexion reflex (VFR) in the ipsilateral hand. This study aimed to assess the effect of unilateral AP at one hand on the VFR in both hands. A systematic study of the relationship between VFR and the force of voluntary contraction with no vibration (Initial Force: IF) has not been reported previously. Hence, this relationship was studied before the present study on AP. VFR was induced by mechanical vibration on the volar side of the middle finger tip with an IF of 10-500 g. VFR was induced consistently with an IF of circa 300 g. Thus, an IF of circa 300 g was applied for VFR induction to study the effect of AP on VFR. A stainless steel needle was inserted into the right LI04 point and remained inserted (in-situ technique) for 10 min. AP at the right LI04 significantly decreased VFR in both hands (% control force of VFR: right, 68%; left, 75%). Unilateral-hand AP influences the bilateral reflex arc of VFR.
Takakura_N2; Ogawa H; Iijima S; Nishimura K; Kanamaru A; Sibuya M; Homma I (1993) Effect of AP at right LI04 on bilateral vibration-induced finger flexion reflex in man: comparison between in-situ and Sparrow Pecking technique. AJCM 21(3-4):213-219. Hanada Coll-Japan Sch of AP, Moxibustion and Physiotherapy, Tokyo. This study compared in 30 healthy adults effect of the Pecking Sparrow (PS) with that of the in-situ (IS) technique of AP on the vibration-induced finger flexion reflex (VFR). Flexion movement of the vibrated finger (VFR), was induced by vibrating the volar side of the middle finger tip. The AP point was LI04 (right side). Both techniques of AP inhibited VFR in the ipsilateral and contralateral sides, but inhibition with PS was significantly more than that with IS (% control force of VFR, mean+SD: with SP right, 62.1+24.6%, left, 60.6+27.9%, with IS right, 74.9+26.6%, left, 78.1+29.5%, p <.0005). SP suppresses facilitation of VFR in the reflex arcs more than IS.
Takakura_N3; Ogawa H; Iijima S; Nishimura K; Kanamaru A; Sibuya M; Homma I (1995) Effect of AP at LI04 on vibration-induced finger flexion reflex in man: comparison between press needle technique, EAP, and in-situ technique. AJCM 23(3-4):313-318. Hanada Coll-Japan Sch of AP, Moxibustion and Physiotherapy, Tokyo, Japan. Effects of press needle technique (PN), EAP, or in-situ technique (IS) on vibration-induced finger flexion reflex (VFR) were examined in 31 healthy adults. VFR, which is tonic finger flexion evoked by vibration applied to the finger tip, was induced by vibrating the volar side of the middle finger tip before and after AP. AP was given at bilateral LI04. The 3 techniques, each studied on separate days, inhibited VFR and there was no significant difference in VFR inhibition among the 3 techniques (% of pre-AP VFR was 72+SE 2.2% after PN, 73+SE 2.4% after EAP, and 76+SE 2.8% after IS). Afferent signals from muscles contracting due to electrostimulation had no significant effect on the reflex arcs of VFR. The intradermal stimulation by AP played a significant role in VFR inhibition.
Takeshige_C1; Luo CP; Hishida F; Igarashi O (1990) Differentiation of AP and non-AP points by difference of associated opioids in the spinal cord in production of analgesia by AP and non-AP point stimulation, and relations between Na and those opioids. AETRIJ 15(3-4):193-209. Dept of Physiol, Showa Univ Sch of Med, Tokyo, Japan. Met-Enk antiserum i.t. abolished APA caused by low frequency stimulation of an AP point (ST36) of rats, but antisera of Leu-Enk and dynorphin (Dyn) did not. Dyn antiserum i.t. abolished analgesia (NAA) produced by stimulation of a non-AP point (NAPS) which was revealed by lesion in the analgesia inhibitory system (AIS), whereas antisera of Met-Enk and Leu-Enk did not. NAA was antagonized by the kappa-receptor antagonist, Mr2266, and analgesia was produced by the kappa-agonist, U50-488H, in the AIS lesioned rats. Potentials in the dorsal periaqueductal central grey (D-PAG) evoked by AP stimulation were antagonized by naloxone and antiserum of Met-Enk, and those in the lateral PAG (L-PAG) evoked by NAPS were antagonized by Mr2266 and antiserum of Dyn. After adrenalectomy, APA, potentials in the D-PAG, and analgesia caused by stimulation (SPA) of the D-PAG were abolished 12 h; and NAA, potentials in the L-PAG, and SPA of the L-PAG were abolished in 24 h. All were then restored 1 h after iv application of 1 ml of 5% NaCl solution. APA and NAA which were augmented for several hours before their abolition after adrenalectomy were not antagonized by naloxone nor M 2266, respectively. However naloxone and Mr2266 did antagonize APA and NAA, respectively, 1 h after treatment with 1 ml of 5% NaCl solution.
Takeshige_C2; Zhao WH; Guo SY (1991) Convergence from the preoptic area and arcuate nucleus to the median eminence in AP and non-AP point stimulation analgesia. Brain Res Bull May 26(5):771-778. Dept of Physiol, Showa Univ Sch of Med, Tokyo, Japan. Lesion of the preoptic area (POA) or medial arcuate nucleus (M-HARN) abolished APA. Potentials in the median eminence (ME) evoked by stimulation of the AP point were not affected by lesion of either the POA or M-HARN alone, but were abolished by concurrent lesion of both. No analgesia was produced by stimulation of the POA. Analgesia produced by stimulation of the M-HARN was abolished by lesion of the POA, and the abolished analgesia was restored by concurrent stimulation of the POA and M-HARN, hence POA and M-HARN outputs might converge in the ME to produce APA. Similar convergence from the anterior arcuate nucleus (A-HARN) and POA to the ME was observed in analgesia (NAA) produced by stimulation of a non-AP point (NAP). 2 pathways diverged from the lateral hypothalamus in the APA afferent pathway and 2 from the lateral periaqueductal central grey (L-PAG) in the NAA afferent pathway. POA potentials evoked by stimulation of the AP point were reversed by naloxone, and those evoked by stimulation of the point were reversed by dexamethasone. ACTH sensitive sites were found in both the L-PAG and the anterior hypothalamus.
Takeshige_C3; Tsuchiya M; Guo SY; Sato T (1991) Dopaminergic transmission in the hypothalamic arcuate nucleus to produce APA in correlation with the pituitary gland. Brain Res Bull Jan 26(1):113-122. Dept of Physiol, Showa Univ Sch of Med, Tokyo, Japan. APA caused by low frequency stimulation of the AP point was abolished by hypophysectomy and adrenalectomy. Termination of APA producing pathway from the AP point to the pituitary was in the medial hypothalamic arcuate nucleus (M-HARN). The origin of the descending pain inhibitory system associated with APA was in the posterior HARN (P-HARN). During AP stimulation, microinjection of 0.5 mg/kg morphine ip, or 0.1 ug beta-End into the P-HARN, restored APA in hypophysectomized rats, and enhanced neuronal activity in the P-HARN that were abolished during AP stimulation. Of the analgesia produced by dopamine or beta-End injected into the P-HARN, that caused by beta-End disappeared after denervation of the M-HARN. The P-HARN neurons that responded to AP stimulation also responded to iontophoretic dopamine, but not to iontophoretic morphine nor ultramicroinjected beta-End. The transmission between the M-HARN and P-HARN may be dopaminergic, and beta-End might presynaptically modulate this transmission. Reduction of sodium ions may have been the reason for abolition of AA after adrenalectomy.
Takeshige_C4; Nakamura A; Asamoto S; Arai T (1992) Positive feedback action of pituitary beta-End on APA afferent pathway. Brain Res Bull Jul 29(1):37-44. Dept of Physiol, Showa Univ Sch of Med, Tokyo, Japan. Potentials in the final sector of the afferent pathway from the AP point were enhanced by 0.5 mg/kg morphine ip without changing the threshold of AP stimulation and greatly decreased by hypophysectomy. The decreased potentials were restored to the control level by morphine (0.5 mg/kg, ip). Potentials evoked in the final sector of the afferent pathway from the non-AP point (NAP) by NAP stimulation after lesion of the analgesia inhibitory system were greatly enhanced by corticotropin (ACTH) (0.25 mg/kg, ip) and greatly decreased by hypophysectomy. Diminished potentials were restored to the control level by ACTH (0.25 mg/kg, ip). Both morphine (0.5 mg/kg, IP) and ACTH (0.25 mg/kg, ip) produced analgesia, but morphine did not affect APA and ACTH did not affect non-AP point stimulation-produced analgesia (NAA). All analgesia, that due to 0.5 mg/kg morphine or 0.25 mg/kg ACTH, APA, and NAA were abolished by hypophysectomy. The abolished APA and NAA were restored by 0.5 mg/kg morphine and 0.25 mg/kg ACTH, respectively. Hence, beta-E and ACTH released from the pituitary by stimulation of an AP point and NAP may act as positive feedback on the APA and NAA afferent pathways, respectively.
Takeshige_C5; Sato T; Mera T; Hisamitsu T; Fang J (1992) Descending pain inhibitory system involved in AP-analgesia (APA). Brain Res Bull Nov 29(5):617-634. Dept of Physiology, Showa Univ Sch of Med, Tokyo, Japan. The descending pain inhibitory system (DPIS) associated with APA, caused by low frequency EAP of an AP point, was identified by the results of lesioning and stimulation procedures previously used to differentiate afferent and efferent paths in rats. The DPIS starts in the posterior arcuate nucleus and descends to the hypothalamic ventromedian nucleus (HVM) from whence it divides into two pathways: one path (serotonin-mediated) descends through the ventral periaqueductal central grey (V-PAG) and then to the raphe magnus (RM). The other (noradrenergic) path descends through the reticuloparagigantocellular nucleus (NRPG) and part of the reticulogigantocellular nucleus (NRGC). The afferent and efferent paths are both present in the RM and NRGC. They were identified separately by means of stimulation-produced analgesia (SPA), produced by stimulation of the separate regions in APA-responders and APA-non-responders, because SPA of these regions in non-responders produced only efferent pathway mediated analgesia. [N.B. Stimulation of the CNS sites produced SPA in both APA-responders and APA-non-responders, indicating that the afferent paths were missing in the non-responders].
Takeshige_C6; Oka K; Mizuno T; Hisamitsu T ; Luo CP; Kobori M; Mera H; Fang TQ (1993) The AP point and its connecting central pathway for producing AP-analgesia (APA). Brain Res Bull 30(1-2):53-67. Dept of Physiology, Sch of Med Showa Univ, Tokyo, Japan. Characteristics of the AP point in producing APA were examined by the inhibition of noxious responses in the brain stem reticular formation, potentials, and neuronal activity in the dorsal periaqueductal central grey (D-PAG), and Electro-APA caused by low frequency stimulation of the AP point. Stimulation of the muscle beneath the AP point was effective in producing APA. APA measured by tail flick, vocalization, and writhing tests was abolished by hypophysectomy, and by icv injection of beta-End antiserum into the 3rd ventricle. The pathway from the D-PAG to the anterior hypothalamus (AA-AH) in the APA afferent pathway from the AP point to the pituitary gland was determined. The lateral hypothalamus, lateral septum, cingulate bundle, dorsal-hippocampus, and habenulo-interpeduncular tract were found, as well as regions previously found, to belong to the APA afferent pathway. A network of divergence and convergence in their rostral and caudal relations was observed. The APA afferent pathway diverges from the D-PAG, converges to the HP, and then projects to the AA-AH.
Wang_H4; Jiang J; Can X (1996) Changes of norepinephrine release in rat nucleus reticularis paragigantocellularis lateralis in AP-analgesia (APA). Inst of AP Research, Shanghai Med Univ, PRC. Adapted from WWW. Norepinephrine (NE) of the nucleus reticularis paragigantocellularis lateralis (RPGL) plays an important role in APA. The aim of this experiment was to study the role of NE in RPGL during APA at presynaptic level by using push-pull perfusion, high performance liquid chromatography with electrochemical detection (HPLC-ECD) techniques. Pain threshold increased significantly after 20 min of EAP, while the level of NE and its metabolite MHPG in the perfusate from the RPGL was markedly decreased. A negative correlation existed between the changes of pain threshold and the release of NE and MHPG. EAP inhibited the release of NE from the RPGL during APA.
Wang_HH2a; Xu SF (1993) Effect of D1 and D2 dopamine receptor antagonists on AP-analgesia (APA). Sheng Li Hsueh Pao Feb 45(1):61-68. Dept of Neurobiology, Shanghai Med Univ, PRC. Highly selective D1 or D2 receptor antagonists were tested in a rabbit skin pain model to study the effect of the subtypes of dopamine receptor on APA. D2 receptor antagonists haloperidol and clozapine iv, potentiated APA. D2 receptor antagonists domperidone and sulpiride and D1 receptor antagonist SCH23390 icv also enhanced APA markedly. The effect of D1 and D2 receptor on APA was discussed.
Wang_HH2b; Zhu YH; Xu SF (1994) [The potentiation effect of haloperidol on the binding of etorphine to brain membranes in APA]. Sheng Li Hsueh Pao Aug 46(4):313-319. Dept of Neurobiol, Shanghai Med Univ, PRC. [3H]-etorphine was used in receptor binding studies on membrane preparation from rabbit brain. Scatchard analysis revealed that rabbit brain had 2 different affinity binding sites. In the high affinity site, the dissociation constant (Kd1) of the control group was 2.57+0.33 nmol/L. When analgesia was induced by haloperidol or AP, the Kd1 values decreased respectively (p <.05) to 1.44+0.03 nmol/L and 1.53+0.05 nmol/L. These Kd1 values further decreased to 1.25+0.03 nmol/L when APA was potentiated by combined action of AP and iv haloperidol (p <.01). Autoradiographic analysis of brain slices showed that the density of opioid receptors in many brain regions, such as N. Caudatus, preoptic lateral area, N. Paraventricularis, N. Centromedianus, Periaqueductal grey, showed significant increase. The upregulation of opioid receptors in rabbit brain may be one of the mechanisms in the potentiating action of haloperidol on APA.
Wang_J6; Cheng ZF (1993) The action of medullary tail-flick related neurons in EAP-analgesia. Sheng Li Hsueh Pao Jun 45(3):299-304. Dept of Physiology, Xi'an Med Univ, PRC. 3 types of cells (off-neurons, on-neurons and neutral neurons) were recorded in the rostral ventromedial medulla (RVM) in lightly anaesthetized rats. Just before the occurrence of tail flick elicited by noxious heat, the on-cells showed a burst of activity while the off-cells exhibited a cessation of discharge. No change of neutral cell activity related to tail flick was observed. EAP at the two BL32 points inhibited tail-flick reflex. This EAP-analgesia affected the spontaneous activity of off- and on-cells in a different way: the discharge of most off-cells was increased significantly (p<.05). Tail-flick-related responses of the both cells were inhibited. The off-cells may be the main efferent neurons in RVM involving in EAP-analgesia.