AP and Neurology
APA AND NEUROLOGY (4/4)
Xia_Y1; Zhang L (1994) The components of somatosensory evoked potentials P250-N350 induced by nervi tibialis posterior stimulation. Chen Tzu Yen Chiu - AP Research 19(2):63-65. Dept of AP, Beijing Univ of TCM. The pain components of SEPs induced by stimulation of the posterior tibial nerves were studied by blocking the bloodflow of the leg in 10 normal adults. SEPs after the painful stimuli (0.1 ms square wave pulse) of the right ankle were recorded from the parietal median (C'Z) and the reference electrode at the Earlobe. A pressure of 80 mm Hg above arterial pressure was given to the right calf by sphygmomanometer. The P250-N350 components (latency 244.2+10.1 ms and 344.2+14.9 ms) of the SEPs persisted and the others disappeared when tactile sensation disappeared but pain existed. The P250-N350 were the pain potentials of nervi tibialis posterior SEPs.
Xiong_K; Zheng P (1990) [The effect of the septal area in APA]. Chen Tzu Yen Chiu 15(1):1-5, 12. Dept of Anatomy, Wannan Med Coll Wuhu, Anhui, PRC. This review summarized some articles on the effect of the septal area in APA. Animal-pain thresholds increased when the septal area was stimulated by EAP, and direct electrostimulation of the septal area markedly inhibited the pain discharges of cells in parafascicular nucleus of thalamus, lateral habenular nucleus, PAG and dorsal raphe nucleus. The septal area plays an important role in APA. Most cholinergic neurons in the septal area are located in nucleus of the vertical limb of the diagonal band (VDB); GABA of the septal area is mainly found in the diagonal band nucleus(td); Dopamine is present in high levels in td and lateral septal nucleus(S1) of septal area; The S1 contain high densities enkephalin-containing neuronal cell bodies and terminals; Also, Substance-P and norepinephrine are also high levels in the septal area. These substance above-mentioned have a relations with APA of septal area. A large number of serotonin-containing neurons are found in the raphe nuclei. The serotonin play an important role in APA. The serotonin-containing neurons in dorsal raphe nucleus project to S1. The fibre connections of the raphe nuclei with the td are reciprocation. The periaqueductal grey is a important structure on pain modulation. It projects to septal area and receives the fibres from S1. A number of adrenergic neurons are located within the locus coeruleus. The locus coeruleus participate pain modulation and APA. The locus coeruleus projects to the septal area.
Xu_R; Guan X; Wang C (1993) [Influence of capsaicin treating sciatic nerve on the pain threshold and the effect of APA of rats]. Chen Tzu Yen Chiu 18(4):280-284. Dept of Neurobiol, Tongji Med Univ, Wuhan, PRC. The model of local application of 1.5% Capsaicin (Cap) on the right sciatic nerve and control of Vehicle (Veh) on the left were used. The influence of Cap on pain threshold, EAP (EA) analgesia and Fluoride-resistant acid phosphatase (FRAP) activity in the dorsal horn of spinal cord were observed. The pain threshold of Cap treatment side rose significantly compared with the control side, FRAP in dorsal horn of spinal cord vanished, and the analgesic effect of EA at GB30 of the Cap treatment side markedly decreased, compared with not only that EA at the control side but also that EA before Cap treatment. The C fibres of the primary afferent participate in the input of pain and EAP analgesic information.
Xu_X; Shibasaki H; Shindo K (1993) Effects of AP on somatosensory evoked potentials: a review. J Clin Neurophysiol Jul 10(3):370-377. Dept of Brain Pathophysiol, Kyoto Univ Faculty of Med, Japan. Although AP has a long history of analgesic effects, the mechanisms underlying its effects are still unclear. Somatosensory evoked potentials (SEPs) were adopted in AP research since the 1970s. Research on the effects of AP on the conventional SEP has given variable results; 2 different opinions concerning the presence or absence of AP effects on the conventional SEP are discussed. Since the conventional SEP is mediated mainly by fast conducting sensory nerve fibres, the conventional SEP methods, especially those for recording short-latency SEP, may be inadequate for studying AP mechanisms. In the case of the long-latency cortical SEP, too few data are available to judge the effects of APA. In studies on the effects of APA on pain-SEPs, APA suppressed the amplitude of pain SEPs (and affected latency also in some trials) in both animals and humans, accompanied by an increased pain threshold. Thus, AP seems to have analgesic effects that are probably related to activation of the antinociceptive system, and application of the pain SEP methods to the study of mechanisms of APA may be promising.
Xu_Z1a; Xu W; Chen Z (1990) [Changes in responses of parafascicular nuclei during adjuvant-induced acute arthritis and effect of AP in the rat]. Chen Tzu Yen Chiu 15(1):77-81, 29. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. We showed earlier that during acute arthritis induced in rats by local intraplanter adjuvant, dramatic alterations in the behavioral responses to noxious stimulation occur. This study observed the responses of parafascicular nuclei (Pf) neurons during acute arthritis and the effect of EAP in rats. Results: 1. Differences between arthritic and normal rats for the whole population of somatosensory neurons were not significant (p >.05); however, nociceptive neurons activated exclusively by noxious stimulation were less in arthritic rats (21/60) than in normal rats (35/46) (p <.01) and nociceptive-non-nociceptive neurons activated by both noxious and non-noxious stimulation were more in the arthritic rat (30/60) than in the normal rat (9/46) (p <.01) and differences in the numbers of non-nociceptive neurons between the 2 groups were not significant. 2. Nociceptive responses of Pf neurons (n=16) in acute arthritic rats were inhibited markedly by EAP at GB39 and BL60. In particular, the inhibitory effect was of great significance (p <.01) during 0-10 and 20-35 min after cessation of EAP. The rats were hyperalgesic during adjuvant-induced acute arthritis and EAP induced a good analgesic effect in acute arthritis. Adjuvant-induced acute arthritis in rats is a good model for research in pain and analgesia.
Xu_Z1b; Xu W; Chen Z (1994) Iontophoretic atropine attenuates the inhibitory effect of stimulating SmI on nociceptive responses of pf neurons. Chen Tzu Yen Chiu - AP Research 19(1):16-19. Inst of AP, China Acad of TCM, Beijing, PRC. Using the techniques of multimicropipette and iontophoresis, we observed whether ACh was involved in the cortical descending modulation of Pf neurons in rats. Inhibition elicited by stimulation of the sensorimotor area (SmI) was attenuated after microiontophoretic atropine; the nociceptive responses of Pf neurons were obviously reduced by microiontophoretic ACh. ACh may be considered as one of the neurotransmitters involved in the descending modulation of pain.
Yang_J1; Song CY; Lin BC; Zhu HN (1992) [Effects of stimulation and cauterization of hypothalamic paraventricular nucleus on APA]. Sheng Li Hsueh Pao Oct 44(5):455-460. Dept of Neurobiol, 2nd Military Med Coll, Shanghai, PRC. The role of hypothalamic paraventricular nucleus (PVH) in APA was investigated by local brain stimulation and cauterization. Electro-, or L-glutamate sodium- stimulation of PVH enhanced the APA-effect of ST36, both in a dose dependent manner. Electrical cauterization of PVH decreased the effect of APA; removal of pituitary had no effect on the enhancing effect by injection of L-glutamate sodium.
Yang_J2; Lin BC (1992) Hypothalamic paraventricular nucleus plays a role in APA through the CNS in the rat. AETRIJ Jul-Sep 17(3):209-220. Dept of Nuclear Med, Nan Fang Hospital, Guangzhao, PRC. This work investigates the effect of hypothalamic paraventricular nucleus (PVN) on APA in the rat. Electrostimulation of PVN or injection of L-glutamate sodium into PVN enhanced the APA effect induced by AP at ST36; electrical cauterization of PVN decreased the effect; Removal of the pituitary did not influence the effect of enhancing APA induced by the injection of L-glutamate sodium into PVN. The PVN may play an important role in APA through the CNS.
Yaun_B; Liu X (1992) [Effect of EAP on the nociceptive responses of SI cortical neurons in the rat]. Chen Tzu Yen Chiu 17(2):90-95. Research Lab of Neurophysiol, Xi'an Med Univ, Shaaxi, PRC. 1. The effect of EAP (EA) on the responses of single SI cortical nociceptive neurons to peripheral natural stimuli were observed in unanesthetized and paralysed rats. 2. After EA, the responses to noxious mechanical and/or thermal stimulation reduced markedly in 14/20 (70%) of neurons tested, and slightly increased or unchanged in the remaining 6 neurons, as compared to the responses before EA. 3. In contrast to the variation of nociceptive responses, the responses to innocuous mechanical stimulation increased in 9 neurons and unchanged in other 9 neurons, while deceased in only 2 neurons. 4. A small portion of the neurons were activated by EA stimulation, while their responses to noxious stimulation were inhibited. 5. It is considered that the selective inhibition of the nociceptive responses of SI cortical neurons might be a part of the mechanisms of APA.
Yonehara_N; Sawada T; Matsuura H; Inoki R (1992) Influence of EAP on the release of Substance-P and the potential evoked by tooth pulp stimulation in the trigeminal nucleus caudalis of the rabbit. Neurosci Lett Aug 142(1):53-56. Dept of Pharmacol, Faculty of Dentistry, Osaka Univ, Japan. The effects of EAP (EAP) on the release of Substance-P (SP) and the responses evoked by tooth pulp stimulation (ST) in superficial layers of the trigeminal nucleus caudalis (Vc-I,II) were studied in rabbits. ST evoked increase in release of immunoreactive SP (iSP). This increase was inhibited by EAP in 9 of 13 animals. The potentials evoked by ST were composed of 2 main components with latency times of ca 4.3 ms and circa 9.4 ms. The latter component, reflecting the excitation of A delta fibres, was significantly inhibited by CP-96,345 (3 mg/kg, iv), an SP antagonist. EAP also inhibited the latter component in 8/11 animals. One of the mechanisms of analgesia induced by EAP is inhibition of stimulus-evoked SP release in the Vc-I,II.
Yuan_B; Pang T; Liu X (1991) [Response properties of SI cortical neurons to EAP and manual AP in the rat]. Chen Tzu Yen Chiu 16(2):79-86. Research Lab of Neurophysiol, Xi'an Med Univ, PRC. Single SI cortical neurons were recorded extracellularly with glass micropipettes, and their response properties to EAP (EA) of contralateral ST36 and ST40, or to manual AP (MA) of ST36 were observed in unanesthetized and paralysed rats. In 46 rats, a total of 474 neurons were isolated in the hindlimb representation area of SI cortex. Among these neurons, 228 responded to peripheral mechanical stimulation, and were classified as cutaneous neurons, deep neurons and cutaneous-deep convergent neurons. 35 of them were identified as nociceptive neurons. Neurons of various sensory neurons and with receptive fields (RFs) located in the contralateral hindlimb responded to EA. Significant difference (p <.01) existed between the stimulation thresholds of cutaneous neurons (2.39+0.27V) and those of deep neurons (4.12+0.48V). There was no significant difference between the thresholds of nociceptive and non-nociceptive neurons. The typical response of SI neurons to single EA stimulation consisted of early discharges with a latency of 11.57+0.39 ms and late train discharges with a latency of 54.79+4.07 ms. A period of inhibition frequently intervened between the 2 groups of discharges. In a small portion of neurons, only a period of inhibition was produced. The responsiveness of neurons decreased markedly when the frequency of repeated EA stimulation was increased from 1 Hz to 50 Hz. Neurons of various sensory modalities responded to MA as well. Judging by RF distribution of the responsive neurons, however, the extent of action of MA was smaller than that of EA.
Zhang_LS; Tang YZ; Zhang ZX (1984) Antagonistic effect of Ca and Mg ions in amygdala on Electro-APA and morphine analgesia in the rabbit. Acta Zool Sin Peking 30(1):32-43.
Zhang_Z; Tu Z; Zhu Z (1990) [Effect of icv injection of thyrotropin releasing hormone on EAP analgesia and the level of cerebral cAMP in rats]. Chen Tzu Yen Chiu 15(2):112-116. Dept Physiol, Fac of Basic Med Sciences, Tongji Med Univ, Wuhan, PRC. Experiments were performed on 42 female albino rats weighing from 180-250 g. The pain threshold (PT) was determined by radiant heat induced tail-flick method. The cAMP levels in various regions of brain were measured by radio-immunoassay. EAP (EA) at bilateral ST36 and SP06 in rats significantly elevated PT, increased the level of cAMP in the hypophysis, while decreased that of septal nucleus. No effects were found in the basal PT and the cAMP levels of the hypophysis and septal nuclei after icv injection of TRH. However, after TRH icv, EA did not elevate PT, but still increased hypophysial cAMP with a decrease in the level of cAMP in the septal nucleus. cAMP may be related to EAP-analgesia in some brain regions, and TRH injected into cerebral ventricles can antagonize EAP-analgesia, but this effect seemed to have no relation to the levels of cAMP of hypophysis, septal nucleus, caudatum, hypothalamus and thalamus.
Zheng_P; Xiong K (1990) [The efferent pathway of the septal nuclei on participation in APA]. Chen Tzu Yen Chiu 15(3):177-180. Dept of Anatomy, Wannan Med Coll Wuhu, Anhui, PRC. The efferent projections of septal nuclei from the brain areas relating to pain in the rat were studied with WGA-HRP and HRP methods. Results: The septal areas project widely to some brain areas relating to pain, for instance, locus coeruleus, raphe nuclei, periaqueductal grey, thalamus, hypothalamus, habenular, amygdaloid complex, cingulate cortex and hippocampus ets, but the projections of medial septal nucleus, lateral septal nucleus and diagonal band nucleus are different. It is possible that these fibre projections are one of the morphological basis of septal nuclei for regulating pain.
Zheng_X1; Xu W; Chen Z (1992) [Corticofugal modulation of somatosensory area II on AP effect in nucleus ventralis posterolateralis of the thalamus]. Chen Tzu Yen Chiu 17(3):156-160. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. In order to explore whether cortical somatosensory area 11 (SII) was involved in descending modulation of the effect of EAP (EA) on nucleus ventralis posterolateralis (VPL), the present study was designed to investigate the influence of topical application of lidocaine at SII on the EA effects in VPL nucleus. Experiments were performed on 23 adult cats anaesthetized with pentobarbital sodium (35-40 mg/kg ip) and immobilized with gallamine triethiodide. The single unit activities of VPL neurons were extracellularly recorded using glass microelectrodes. Results: 1. The nociceptive responses of VPL were obviously attenuated after EA at GB30 and GB34. The difference was statistically significant at 0-10 min after cessation of EA (n=13, p <.001 or p <.05), then it was gradually recovered. EA inhibited the nociceptive responses of VPL neurons. 2. The inhibitory effect of AP on nociceptive responses were reduced or abolished after topical application of lidocaine (n=14, p >.05). However, it exerted marked inhibition at 0-10 min after cessation of EA in the saline control group (n=14, p <.05). There was a statistical difference between these 2 groups (p <.05). SII was involved in descending modulation of AP effect in VPL nucleus.
Zheng_X2; Chen Z; Xu W; Shi H (1994) Involvement of glutamate in corticofugal modulation of intralaminar nuclei from SII via motor cortex in AP-analgesia (APA). Chen Tzu Yen Chiu - AP Research 19(1):11-15. Inst of AP, China Acad of TCM, Beijing, PRC. This was a study of the effect of glutamate on cortical somatosensory area II (S II) producing descending modulation of intralaminar nuclei (ILN) via the motor cortex (MCtx) in APA. The glutamate antagonist glutamate diethylester (GDEE) or saline was applied topically at MCtx in 17 cats. Single unit activities of ILN neurons were recorded extracellularly. Nociceptive responses of ILN neurons were attenuated by stimulating S II after topical application of saline at MCtx. However, the inhibitory effect of stimulating S II in the same neurons was reduced after application of GDEE. There was a significant difference at 0-1 h after the stimulation between the two groups (n=10, p <.05). The inhibitory effect of EAP on nociceptive responses was reduced after topical application of GDEE, while marked inhibition was shown at 0-10 h after cessation of EAP in the saline control group (n=11, p <.05). The results, and the finding that EA activated most S II neurons, showed that glutamate released from S II to MCtx may be involved in corticofugal modulation of ILN from S II via MCtx in APA.
Zhou_L2a; Tian Q; Jiang J; Wu G; Cao X (1991) [Effect of electro-stimulation and lesion of N reticularis paragigantocellularis lateralis on APA in rats]. Chen Tzu Yen Chiu 16(2):103-107. Dept of Neurobiol, Shanghai Med Univ, PRC. This study aimed to investigate the role of the reticularis paragigantocellularis lateralis (RPGL) in APA. Tail-flick response to electrostimulation of the tail skin was taken as index of pain response. The first part of the study consisted of 4 groups: 1=surgical control, n=14; 2=EAP, n=14; 3=electrostimulation of RPGL, n=14; 4=EAP + simultaneous stimulation of RPGL, n=8). The pain threshold in group 1 was stable during the experiments, but increased significantly after EAP (p <.001) and/or brain stimulation (p <.01; p <.001). Mean pain threshold of group 4 increased much more than that of groups 2 and 3 (p <.001, p <.01). In part 2, a unilateral electrical lesion of the RPGL (n=12, p <.01) significantly reduced the effect of EAP. Electrical stimulation of RPGL enhances EAP-analgesia, but an RPGL-lesion reduces it. The RPGL plays a role in APA.
Zhou_L2b; Jiang JW; Wu GC; Cao XD (1993) [Changes of endogenous opioid peptides level in RPGL during AP-analgesia (APA)]. Sheng Li Hsueh Pao Feb 45(1):36-43. Dept of Neurobiology, Shanghai Med Univ, PRC. Assessed by push-pull perfusion technique and RIA of neuropeptides, release of Leu-Enk from the RPGL was significantly higher after EAP for 20 min, than in the control group (p<.05) but no significant changes were found in the EAP group that had poor analgesia. Changes of release of Leu-Enk or beta-End correlated positively with increase of pain threshold. The release of DynA1-13 was barely significant (p >.05). APA increased the release of Leu-Enk and beta-End in the RPGL.
Zhou_L2c; Wu GC; Cao XD (1995) Role of opioid peptides of rat's nucleus reticularis paragigantocellularis lateralis (RPGL) in AP-analgesia (APA). AETRIJ Apr-Jul 20(2):89-100. Dept of Neurobiology, Shanghai Med Univ, PRC. We studied the role of the RPGL and its endogenous opioid peptides in APA using techniques of brain stimulation and lesion, microinjection, push-pull perfusion and RIA. Electrostimulation of the RPGL increased pain threshold and enhanced the effect of Electro-APA; lesion of the RPGL reduced the effect of APA. Microinjection of naloxone (5 ug/0.5ul/2min) into the RPGL partially reversed the effect of APA and the reversal effect of naloxone was dose-dependent. Release of Leu-Enk and B-endorphin (B-EP) from the RPGL in the APA group was significantly higher than that in the control group (p <.05). Correlations between the changes of release of Leu-Enk, B-EP, and the increase of pain threshold, were positive. The RPGL may play an important role in APA. Activation of the RPGL and the endogenous opioid peptides within it enhance the effect of APA.
Zhou_Y4; Sun YH; Shen JM; Han JS (1993) Increased release of immunoreactive CCK-8 by EAP and enhancement of EAP-analgesia by CCK-B antagonist in rat spinal cord. Neuropeptides Mar 24(3):139-144. Neuroscience Research Centre, Beijing Med Univ, PRC. In the CNS, CCK octapeptide (CCK-8) acts as a potent anti-opioid neuropeptide. It hinders opioid analgesia and facilitates opioid tolerance. EAP markedly increased CCK-8 immunoreactivity (ir) in the perfusate of the rat spinal cord. The increase of CCK-8-ir was most marked in response to EAP of 100 Hz and 15 Hz, and less marked in response to EAP of 2 Hz. Since CCK-8 possesses potent anti-opioid activity at the spinal level, blockade of the spinal CCK effect would be expected to potentiate EAP-analgesia, which is known to be opioid-mediated. Intrathecal (i.t.) injection of CCK-8 antagonist L-365260 per se did not affect tail flick latency (TFL) significantly, yet it potentiated EAP-analgesia in a dose- and frequency- dependent manner. The potentiation was most marked at a dose range of 2.5-5.0 ng (i.t.) and at a frequency rank order of 100 Hz > 15 Hz > 2 Hz. Increased release of CCK-8 after EAP may limit the effect of opioid peptides; CCK-8 receptor mediates the anti-opioid effect of CCK-8 in rat spinal cord.
Zhu_CB; Li XY; Zhu YH; Xu SF (1995) Binding sites of mu receptor increased when APA was enhanced by droperidol: an autoradiographic study. Chung Kuo Yao Li Hsueh Pao Jul 16(4):311-314. Dept of Neurobiol, Shanghai Med Univ, PRC. AIM: To study if mu receptor participates in the process of potentiation of droperidol (Dro) on APA. METHODS: Autoradiographic technic was used. Ohmefentanyl, a highly selective ligand of mu receptors, was used in radio-receptor binding assay in Sprague-Dawley rat brain sections. Results: The binding sites of [beta-3H, p-benzoyl-3H]ohmefentanyl were increased greatly in many nuclei of rat brain after APA, and were further increased when APA was enhanced by Dro. Higher increase was seen in caudate nucleus, accumbens, PAG, interpeduncular nucleus, amygdala (p <.01 v rats treated with EAP alone); moderate increase was noted in thalamus, lateral area of hypothalamus, spinal dorsal horn (p <.01 or 0.05); slight increase appeared in septum, preoptic area, hippocampus, substantia nigra (p <.05). Conclusion: Mu opioid receptors mediated the Dro-induced enhancement of APA.
Zhu_J; Xia Y; Cao X (1990) [Effects of noradrenaline and dopamine in preoptic area on APA]. Chen Tzu Yen Chiu 15(2):117-122. Dept of Neurobiol, Shanghai Med Univ, PRC. Previous work has shown that activation of catecholamine in the preoptic area is to the disadvantage of APA. In this work microinjection and push-pull perfusion as well as HPLC-ECD were used to observe the effect of noradrenaline and dopamine in this area on APA. Results: Microinjection of noradrenaline (0.5 ug unilaterally) into the preoptic area attenuated APA; dopamine (2 ug unilaterally) had no effect on APA. During APA, the levels of noradrenaline and MHPG in the perfusate from the preoptic area decreased markedly but dopamine did not change significantly. Activating noradrenaline, but not dopamine, had antagonistic effect on APA.
Zhu_JM; He XP; Cao XD (1990) [Changes of releases of beta-End-like immunoreactive substances and noradrenaline in rabbit's preoptic area during APA]. Sheng Li Hsueh Pao Apr 42(2):188-193. Dept of Neurobiol, Shanghai Med Univ, PRC. RIA and HPLC-ECD were used respectively to detect beta-End-like immunoreactive substances (beta-EPIS), noradrenaline and 3-methoxy-4-hydroxyphenyloglycol (MHPG), a noradrenaline metabolite, in the perfusate from the rabbit's preoptic area before and after 10 min of EAP (EA). It was found that, the level of beta-EPIS in the perfusate increased during APA, while those of noradrenaline and MHPG decreased. A negative correlation (r=-.831; p <.05) was shown between the changes of beta-EPIS and MHPG levels during APA, indicating that beta-End may be related to the inhibition of noradrenaline release during APA.
Zhu_JM; Li KY; Cao XD (1990) [Effects of destruction of preoptic catecholaminergic nerve terminals on APA]. Sheng Li Hsueh Pao Apr 42(2):135-140. Dept of Neurobiol, Shanghai Med Univ, PRC. The effect of microinjection of 6-hydroxydopamine into the preoptic area was studied to observe the effect of destruction of catecholaminergic terminals in the preoptic area on APA. It was shown that the analgesic effect of AP was significantly enhanced in 6-hydroxydopamine treated group on d 2 and d 4 after injection as compared with those before injection or those in control group. The fluorescence of catecholamine terminals in the preoptic area disappeared almost completely on d 4 after injection, and did not restore on d 10. Reduction of catecholamine level in the preoptic area may enhance APA.
Zhu_L; Li C; Yang B; Ji C; Li W (1990) The effect of neonatal capsaicin on APA: to evaluate the role of C fibres in APA. Chen Tzu Yen Chiu 15(4):285-291. Inst of AP, China Acad of TCM, Beijing, PRC.
Zhu_L; Li C; Ji C; Li W (1993) [The role of OLS in peripheral APA in arthritic rats]. Chen Tzu Yen Chiu 18(3):214-218. Inst of AP and moxibustion, China Acad of TCM, Beijing, PRC. We showed previously that opiate-like substance (OLS) is involved in the central mechanism of APA in arthritic rats. In this paper, the role of OLS in peripheral mechanism of APA is studied further. 24 h after sc injection of Freund's adjuvant into the right ankles, acute arthritis with typical symptoms developed in all rats. After AP needling at GB30 for 10 min, the pain threshold (PT) rose by 42.3% (p <.05) in the inflamed ankles and by 5.6% in the non-inflamed ones. A dose of 250 and 100 ug naloxone (Nx) iv completely and partially (49.6%) blocked AA, respectively. Nx by local (icv ?) injection (100 ug, even 20 ug) completely antagonized APA. After morphine iv (10, 5.0, 2.5, 1.25 mg/kg), PT rise was dose-related, and PT was raised by 86.5+22.7% in the affected ankles and by 32.9+14.9% in the normal ankles at a dose of 5 mg/kg. Opiate receptors in the inflamed area seem to be sensitized and activation of the endogenous opiate system may be involved in APA. AP may enhance the release of peripheral OLS, which can act at the sensitized opiate receptors, leading to more potent analgesic effect in the inflamed area.
Zhu_LX; Zhao FY; Cui RL (1991) Effect of AP on release of substance P. Ann NY Acad Sci 632:488-489. Dept of Physiology, China Acad of TCM, Beijing, PRC.
Zhu_LX; Li CY; Ji CF; Yang B; Li WM (1993) [The role of Substance-P and somatostatin in AP and moxibustion-induced postsynaptic inhibition]. Chen Tzu Yen Chiu 18(4):290-295. Inst of AP and moxibustion, China Acad of TCM, Beijing, PRC. Our previous work indicated that AP and moxibustion (heating AP points with a special lamp) could inhibit the tail flick reflex and the nociceptive response of dorsal horn neurons. In the present study the role of somatostatin (SS) and Substance-P (SP) in AP and moxibustion-induced postsynaptic inhibition was studied further. The experiments were performed on male adult Wistar rats. The antidromic action potential (AAP) induced by cervical cord stimulation was recorded extracellularly at lumbar cord (L3-4). AAP latency was used to represent the excitability of postsynaptic projecting neurons. The effects of AP (0.5 ms, 3.3 Hz, 2 mA) for 5 min or moxibustion (the temperature up to 45-46oC) for 6 min at GB30 points on the latency of AAP were observed. And then the effects of topical administration of SS or SP antiserum on either AP or moxibustion-induced postsynaptic inhibition were observed. Results: AAP latency was markedly prolonged by AP and moxibustion. The maximal prolongation was 0.196+0.071 ms (n=12, p <.02) and 0.176+0.062 ms (n=11, p <.02) respectively. After topical administration of SS antiserum (1:40, 10 uL), AAP latency was prolonged slightly by either AP or moxibustion. The maximal prolongation (0.041+0.029 ms and 0.016+0.020 ms) was significantly reduced by SS antiserum (p <.05). While pretreated with SP antiserum, the latency was still prolonged by moxibustion (0.142+0.067 ms), but not by AP (-0.003+0.046 ms). Postsynaptic inhibition may be involved in both APA and moxibustion analgesia. The former is predominately mediated by SP and partially by SS, while the latter mainly by SS but not by SP.
Zhu_S; Shi F; Liu Z; Jiang J (1990) [Autoradiographic visualization on the role of central 3H-5-HT in APA]. Chen Tzu Yen Chiu 15(4):269-273. Suzhou Med Coll, PRC. The role played by central 5-hydroxytryptamine (5-HT) in EAP analgesia has been studied in rats by means of autoradiography with isotopic tracers 3H-5-HT. The purpose of the present study is to determine the localization of 3H-5-HT in the midbrain raphe nuclei and in the mesencephalon aqueduct as well as periaqueductal grey matter. Parallel experiments were studied by freezing microautoradiographic method and histo-fixative microautoradiographic method. The analgesia effect of AP can be enhanced or lowered by the increment or the decrement of the 5-HT level in the midbrain raphe nuclei and in the mesencephalon aqueduct as well as periaqueductal grey matter. When the rats were subjected to EAP analgesia, the microautoradiographic intensities of 3H-5-HT both in the midbrain raphe nuclei and in the areas of mesencephalon aqueduct were significantly increased. The release of 5-HT in these regions of the brain was accelerated during APA. Midbrain raphe nuclei and the mesencephalon aqueduct as well as the periaqueductal grey matter are closely related to APA. 5-HT in these areas may be one of the most important neurochemical agents mediating APA.
Zou_T; Liu X (1993) [The influence of pyramidal tract pathway of sensorimotor cortex on the effects of APA on NRM neurons]. Chen Tzu Yen Chiu 18(1):29-32, 36. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. The experiment was to study whether the effects of EAP (EA) on neurons in nucleus raphe magnus (NRM) were influenced after lesion of bilateral pyramidal tracts (PT) in the rats. Unit discharges of NRM were recorded extracellularly with glass microelectrodes and their nociceptive responses were induced by trains of electrostimuli to the tail. Only neurons excited by noxious stimulation of the tail were researched. 1. The effects of EA at bilateral ST36 points on 31 NRM neurons were observed in control group. EA had a tendency to activate NRM neurons, but inhibited obviously nociceptive response of the neurons at 0-30 min (p <.01). The effects of EA of PT control group (PT exposed and kept intact) were recorded on 8 units in NRM. EA had a tendency to activate the neurons, but inhibited obviously nociceptive response of the neurons and decreased nociceptive response rate 25.3+8.7% at 0 minute (n=8, p <.05) 3. EA after the PT lesion, it obviously inhibited nociceptive response of the neurons in NRM at 0-20 min (n=9, p <.01-0.05). It inhibited nociceptive response of all the neurons and decreased nociceptive response rate 57.8+11.6% at 0 minute (p <.01). The effect was larger than the effect of EA of PT control group and increased 32.5% at 0 minute (p <.05) than this. It also increased the effect of EA activating the neurons than PT control group. SM may influence the effect of EA analgesia, which involves in both PT and extrapyramidal system (EPS).