AP and Neurology
APA AND NEUROLOGY (2/4)
Gao_M; Li Q; Zhang J; Liu Y (1990) [Effect of changing the functional state of frontal cortex by GABA on the AP effect of PAG neurons]. Chen Tzu Yen Chiu 15(4):264-268. Dept of Physiol, Research Lab of APA Mechanism, Guangxi Med Coll. This was a study of the corticofugal modulation of nucleus periaqueductal grey (PAG) after EAP by topical application of GABA on the frontal cortex. Rabbits were restrained and immobilized with gallamine. Electrostimulation of the n. suralis was used as the noxious stimulation. Single unit activities of PAG neurons were record with glass microelectrodes extracellularly. Bilateral ST36 and GB30 were stimulated by EAP. GABA was applied topically by means of 3 x 3 mm2 filter paper and placed on the frontal cortex. The responses of most PAG neurons evoked by noxious stimulation were inhibited after simple EAP. On the contrary, the AP effect on PAG neurons was abolished when GABA was applied on the frontal cortex. However, the effect of saline control resembled that of simple AP. Corticofugal modulation from the frontal cortex may play a role in APA.
Guan_X; Liang X; Liu X (1990) [Acetylcholine and the primary input of AP sensation: influence of peripheral ACh on the role of EAP analgesia]. Chen Tzu Yen Chiu 15(2):136-139. Dept of Neurobiol, Tongji Med Univ, Wuhan. In order to investigate the correlation between the peripheral ACh and the primary input of AP sensation, in the paper the cholinesterase inhibitor, Neostigmine and the ACh synthesis blocker, Hemicholine, which are unable to pass through blood brain barrier, and ACh were used as tools to increase or decrease the level of ACh in peripheral nerve system of rats. Results: 1.The effect of EAP analgesia was enhanced in a dose-related way by sc injection of neostigmine. 2. ip injection of Hemicholine markedly inhibited the influence of EAP analgesia. 3. Injection of ACh in combination with neostigmine immediately reversed the suppression of EAP analgesia by hemicholine. But could not reverse by neostigmine alone. The effect of EAP analgesia and the primary input of AP sensation were significantly related to the level and content of peripheral ACh.
Guan_X; Wang C; Yu B; Liang X; Zhang Y; Zeng X; Liu X; Shi J; Ai M (1991) [Research on the relationship between central ACh and APA]. Chen Tzu Yen Chiu 16(2):129-137. Dept of Research on APA & Neurobiol, Tongji Med Univ, Wuhan, China. The article systematically reported our physiological and biochemical work on the relationship between central ACh and APA. AP on AP points produced analgesia. APA increased ACh levels in CSF and brain, increased AChE activities in brain. ChE inhibitor reinforced APA and ACh-synthesis-inhibitors inhibited APA, which inhibition was reversed by injection of ACh and chlorocholine. M-AChR antagonists also inhibited APA. APA increased the turnover rate of ACh in diencephalon, caudate nucleus and spinal dorsal horn. Variation of metabolic dynamics was discussed in relation to published literature.
Guoxi_T (1991) The action of the visceronociceptive neurons in the posterior group of thalamic nuclei: possible mechanism of APA on visceral pain. Kitasato Arch Exp Med Apr 64(1):43-55. Lab of Neurophysiol, China Med Univ, Shenyang. Microelectrode and stereotaxic technique were used to record extracellular potentials of the neuron in posterior group of thalamic nuclei (PO). To study the action of some neural structures in the brain, we also applied the method of conditioning-testing stimulation. We found not only somatic nociceptive but visceronociceptive neurons existed in PO. The features of the unit response (latency,discharges and its noxious properties) were studied. Stimulation of S1, cingulate gyrus, caudate nucleus, accumbens, amygdala, habenula, VPL, PAG and substantia nigra caused inhibition of nociceptive neurons in PO. Owing to emerge and recover, the inhibition can be divided into 3 phases: prompt, continued and delayed. All these inhibitions except VPL, Cad and SN (no observation), were reversed by Naloxone. Both stimulation of somatic peripheral nerve fibres and EAP of ST36 of the cat produce suppression of nociceptive neuron in PO. The mechanism of inhibition from the above neural structures of the brain was also discussed.
Han_Y; Yin Q (1992) [Electrophysiological observation on the role of the hypothalamic paraventricular nucleus in APA]. Chen Tzu Yen Chiu 17(3):161-165. Lab of Neurobiol, Suzhou Med Coll, Jiangsu. PRC. In this experiment, the role of PVN in APA was further investigated with electrophysiological technique. Unit discharges were recorded extracellularly in Wistar rats. Noxious stimulation was applied to the sciatic nerve and EAP was given at ST36 and SP06. Totally 82 units were recorded successfully from PVN. 49 units of them reacted to EAP with excitatory (14), inhibitory (23) or on significant effect (12). Various types of reactions including excitation (12), inhibition (6), excito-inhibition (4) or inhibito-excitation (3) were observed on 43 units during noxious stimulation of sciatic nerve. The remainder 18 units had no significant reaction. After EAP those units reacting with excitatory effect on noxious stimulation decreased their firing rate, and those with inhibitory effect increased their firing rate. The duration of nociceptive reaction was shortened after EAP in both types of units. EAP may influence the activities and decrease the nociceptive reactions of PVN neurons. This is electrophysiological evidence of the involvement of PVN in APA.
Huang_K; Xia-L; Rosenfeld-JP (1990) Effects of AP on activity of nociresponsive trigeminal nucleus caudalis (TNC) and a comparison with the effects of nanoinjecting Met-enkephalin (ENK) into the midbrain periaqueductal grey (PAG) or bulbar nucleus reticularis paragigantocellularis (PGC). Chen Tzu Yen Chiu 15(4):274-279. Inst of AP and Moxibustion, China Acad of TCM, PRC.
Huang_Z; Liu N; Zhong S; Lu J; Zhang N (1991) [The role of nucleus tractus solitarii (NTS) in AP inhibition of visceral-somatic reflex (VSR)]. Chen Tzu Yen Chiu 16(1):43-47. Dept of Physiol, Chongqing Univ of Med Sciences. Experiments were carried out on 164 rabbits. The transmission of abdominal vagal impulses and the mechanism of inhibitory effect by AP systematically were investigated. 1) Electrostimulation (single pulse of 20 V, 0.5 ms) of abdominal vagus nerve (AVN) produced 2 kinds of potential on cervical vagus nerve: the fast wave (10.4-24.4 M/s) and the slow wave (0.9-1.7 M/s), the later was more stable. 2) In dorsal medulla oblongata the 'M' shaped evoked potentials with long duration (100 ms or so) were recorded. Afferents from AVN are mainly transmitted through the small fibres and multi-synaptic connections in Medulla. 3) 281/301 response units (93.6%) concentrated in NTS and adjacent regions. This result was also confirmed by injection of Horseradish Peroxidase (HRP) in the trunk of AVN. 4) On 24 awake rabbits the VSR were elicited by strong stimulation of AVN. EAP (EA) at ST36 inhibited VSR, an effect lasted over 20 min. This inhibitory effect of EA was reversed partly by Naloxone (0.5 mg/kg iv) and was attenuated after lesion (DC 0.5 mA, 1 min.) of NTS. In conclusion, NTS plays an important role in suppression of VSR by EA (p <.01).
Ignatov_IuD; Vasil'ev IuN; Kolchin VV; Amelin AV; Li Ch Kh (1991) [The analgetic activity of antidepressants and their influence on the pain-relieving effect of AP]. Farmakol Toksikol May-Jun 54(3):12-14. The analgesic properties of Soviet-made antidepressants pyrasidol, incazan, tetrindol as compared with amitriptyline and their influence on APA were studied in rat experiments by using increasing intensity of electrostimulation of the tail root. Single and subchronic (6 d) administration of all the studied drugs had analgesic actions. Pyrasidol exerted the most pronounced effect. The antidepressants enhanced the analgesic effect of EAP, in particular during activation of the points of general action (such as LI04, ST36 etc). Pyrasidol medication had the greatest synergistic effect on APA.
Janssens_LAAa2; Rogers PAM; Schoen AM (1988) APA: a review. Vet Rec 9 Apr 122(15):355-358. Oudestraat 37, Wilryk, Belgium.
Jeong_Y; Baik EJ; Nam TS; Paik KS (1995) Effects of iontophoretically applied naloxone, picrotoxin and strychnine on dorsal horn neuron activities treated with high frequency conditioning stimulation in cats. Yonsei Med J Sep 36(4):336-347. Dept of Physiology, Yonsei Univ Coll of Med, Seoul, Korea. TENS, AP-needling, and EAP are useful non-ablative methods in Med practice for relief of pain. These procedures seem to work by causing an increased discharge in afferent nerve fibres which in turn modifies the transmission of impulses in pain pathways. The mechanism of analgesic effect via these procedures varies, depending on the stimulating parameters. For example, the endogenous opioid system is profoundly related to the mechanism when peripheral TENS is applied with parameters of low frequency and high intensity. However, when stimulated with parameters of high frequency and high intensity, the reduced activity of dorsal horn neurons is only slightly reversed by a systemic injection of naloxone, a specific opiate antagonist. Thus, the present study examined the neurotransmitter that concerns the mechanism of peripheral nerve stimulation with parameters of high frequency and high intensity. We used an iontophoretic application of antagonists of possible related neurotransmitters. Via a microelectrode at the lumbosacral spinal cord, dorsal horn neuron activity, evoked by squeezing the peripheral cutaneous receptive field, was recorded as an index of pain. Naloxone, picrotoxin and strychnine were applied at 200nA during a period of conditioning TENS. The effects of these drugs on the change of dorsal horn neuron activities were noted. Spontaneous activity of dorsal horn neurons increased in the presence of glutamate and decreased with GABA. It did not change with naloxone, picrotoxin or strychnine. When naloxone was applied iontophoretically during peripheral TENS, the analgesic effect was not statistically significant less than that of the control group. When picrotoxin was applied iontophoretically during TENS, the analgesic effect was reduced. When strychnine was applied, the analgesic effect was reduced but not significantly. The GABAergic system may have been partially related in the analgesic action of peripheral TENS of high frequency and high intensity.
Jiang_M; Liu X (1994) The lesion of somatosensory area II of cerebral cortex reducing the effects of EAP of ST36 on nucleus raphe magnus in rats. Chen Tzu Yen Chiu - AP Research 19(1):4-7. Inst of AP and Moxibustion, China Acad of TCM Beijing, PRC. This work was to study the influence of lesion of Sm II on effects of EAP upon nucleus raphe magnus (NRM). The experiments were performed on rats. The unit discharges of NRM neurons and their responses to noxious stimulation on tail tip were recorded extracellularly with glass microelectrode. The excitatory neurons of NRM were chosen and assigned to 2 groups: 1=Control, before lesion of bilateral Sm II (n=10) and; 2=After the lesion (n=17); two neurons of this group were also observed before lesion. EAP at ST36T activated the neurons in the control group before the lesion of Sm II. Their increased spontaneous discharge in 0-10 min and at 20 min, and decreased nociceptive response in 0-25 min were statistically significant.
Jun_Y (1992) [Effect of AP on the levels of vasopressin and oxytocin in the rat]. Chen Tzu Yen Chiu 17(3):217-20. Dept of Nuclear Med, Nan Fang Hospital, Guangzhou. This work was to investigate the change of the levels of vasopressin and oxytocin during AP in rats. AP changed arginine vasopressin an oxytocin immunoreactivity in many regions of rat brain. Arginine vasopressin and oxytocin may participate APA through the CNS.
Kaliuzhnyi_LV; Kozlov AIu (1991) [Action of an enkephalinase blocker on the effect of AP in AP sensitive and resistant rabbits]. Biull Eksp Biol Med Dec 112(12):571-573. DPA injection did not change the SEP in response to tooth pulp electrostimulation in unanesthetized AP-sensitive rabbits. However, it prolonged the analgetic effect of Ear-EAP stimulation 15 Hz expressed by decreasing of the amplitude of N1P2 component SEP. In AP-resistant rabbit DPA injection induced analgetic effect which was enhanced and prolonged by Ear-AP stimulation. Recovery of pain sensibility after APA may be determined by enkephalinase's mechanism activation which is activated permanently in AP-resistant rabbits.
Kaliuzhnyi_LV; Fedoseeva OV (1990) [Angiotensin mechanism of Ear-AP dental analgesia]. Biull Eksp Biol Med Jul 110(7):3-5. Ear-EAP stimulation at 15 Hz decreased the amplitude of SEP 2nd component in response to the tooth pulp electrostimulation in unanesthetized rabbits. The effect was blocked by iv injection of naloxone but not by icv injection of saralasin. The same effect of Ear-EAP stimulation at 100 Hz was blocked by saralasin, was increased by angiotensin II, was diminished by methysergide but was not changed by naloxone. An angiotensinergic antinociceptive mechanism of dental pain may be activated by Ear-EAP stimulation at 100 Hz.
Kasahara_T; Wu Y; Sakurai Y; Oguchi K (1992) Suppressive effect of AP on delayed type hypersensitivity to trinitrochlorobenzene and involvement of opiate receptors. Int J Immunopharmacol May 14(4):661-665. Dept of Pharmacol, Sch of Med, Showa Univ, Tokyo, Japan. We reported previously that EAP at GV04 in mice either enhanced or suppressed the delayed type hypersensitivity (DTH) to 2,4,6-trinitrochlorobenzene (TNCB, picryl chloride) depending on the time of treatment. We report here the suppression of the efferent phase of DTH to TNCB by EAP in mice. In male BALB/c, C57BL/6 and ddY mice, 7-9 wk-old, significant suppression of the DTH occurred when EAP had been applied once/d for 3 d consecutively before TNCB challenge. When EAP had been applied once only, significant suppression also occurred. EAP at another point (at a middle area of the femoral muscle) failed to suppress the DTH to TNCB. This EAP-evoked DTH suppression was blocked dose-relatedly by pretreatment by iv naloxone hydrochloride. Opioid receptor-mediated mechanisms may be involved in this immune response.
Kashiba_H; Ueda Y (1991) AP to the skin induces release of Substance-P and calcitonin gene-related peptide from peripheral terminals of primary sensory neurons in the rat. Dept of Physiol, Kansai Coll of AP Med, Osaka, Japan. AJCM 19(3-4):189-197. We examined immunohistochemically the short term effects of EAP to the skin on Substance-P (SP)- and calcitonin gene-related peptide (CGRP) containing- primary sensory neurons in the rat. Immunoreactivity to SP and CGRP in these neurons at the treatment site decreased after 30 min of EAP. EAP induces release of SP and CGRP from peripheral terminals of primary sensory neurons.
Kawashima_Y; Toma S; Nakajima Y (1991) Attenuation of somatosensory evoked potentials by AP and tactile skin stimulation in man. Brain Topogr Fall 4(1):37-46. Dept of Physiol, Sch of Med, Chiba Univ, Japan. The effects of AP and tactile skin stimulation on somatosensory evoked potentials (SEPs), elicited by the median nerve stimulation, were investigated in healthy subjects. AP needles were inserted into either LI04 + LI11, LI04 + TH05, or LI11 ipsilateral to the median nerve stimulation. Tactile skin stimulation was applied to either the ulnar side of the palm, or the dorsal surface of the hand or forearm ipsilaterally to the nerve stimulation. It was found that AP significantly suppressed the amplitude of P22 and P40, and that the tactile skin stimulation of the ulnar side of the palm significantly suppressed the amplitude of P22 and P40, but that the peak latencies were not affected. Dipole tracing analysis showed that the location and vector direction of P22 were unchanged but the vector moment of P22 was changed by both AP and tactile stimulation. The suppressive effect of AP and skin stimulation on P22 may be due to afferent inhibition in the somatosensory cortex. Although the suppressive mechanism of P40 by tactile skin stimulation seemed to be similar to that of P22, the suppression of P40 by AP appeared to include different mechanisms.
Kishioka_S; Miyamoto Y; Fukunaga Y; Nishida S; Yamamoto H (1994) Effects of a mixture of peptidase inhibitors (amastatin, captopril and phosphoramidon) on Met-Enk-, beta-End-, dynorphin-(1-13)- and EAP-induced antinociception in rats. Jpn J Pharmacol Nov 66(3):337-345. Dept of Pharmacology, Wakayama Med Coll, Japan. The effects of a mixture of 3 peptidase inhibitors (PIs), amastatin, captopril and phosphoramidon, on Met-Enk-, beta-End-, dynorphin-(1-13) (Dyn)- and EAP- induced antinociception were compared in rats. EAP was performed by passing electric pulses (3 Hz, 0.1 ms duration, for 45 min) through AP needles inserted into LI04. The antinociceptive effect was estimated by the hind paw pressure test. The antinociceptive effects of Met-enk and beta-End injected icv or i.t. and of Dyn injected i.t. were clearly potentiated by the PIs pretreated by the same routes as used to inject opioid peptides. The antinociceptive effects of Met-Enk, beta-End and Dyn injected icv were also potentiated significantly by i.t.-PIs. PIs injected into the PAG potentiated EAP antinociception. However, the EAP effect was not affected by i.t.-PIs and was rather attenuated by icv-PIs. Met-Enk hydrolysing enzymes were involved in the degradation of not only Met-Enk but also beta-End and Dyn in the rat CNS; Met-Enk and beta-End acted on both supraspinal and spinal sites, while Dyn acted only on the spinal site; EAP antinociception was mediated by supraspinal Met-Enk and/or beta-End; EAP activated an anti-opiate peptide system, susceptible to Met-Enk hydrolysing enzymes.
Kumar_A; Tandon OP; Dam S; Bhattacharya A; Tyagi KK (1994) Brainstem auditory evoked response changes after EAP therapy in chronic pain patients. Anaesthesia May 49(5):387-390. Dept of Anaesthesiol and Critical Care, Univ Coll of Med Sciences, Delhi, India. Brainstem auditory evoked responses were recorded in 17 patients with chronic pain who had been given EAP therapy. The absolute peak latencies of waves I to V, and interpeak latencies and amplitudes of waves I and V were analyzed before EAP and compared with values obtained during EAP and 5 min after its termination after one, 5 and 10 sittings. At these sittings the intensity of pain was recorded with the help of a 100 mm visual analogue scale. Each patient had 10 sessions, at 2 d intervals. The absolute peak latencies of waves I, II, and III were delayed significantly (p <.05) after 5 and 10 sittings and amplitudes of wave V decreased significantly (p <.05) after 5 and 10 sittings. Visual analogue scores also decreased significantly (p <.01) during these sittings. It was established that before and after 10 sittings of EAP, there was a significant positive correlation between visual analogue scores and the amplitude of wave V (p <.01). There was a negative correlation between visual analogue scores and absolute peak latencies of wave III at 1, 5 and 10 sittings, suggesting that there is a definite interaction between the EAP neural mechanism and the generators of brainstem auditory evoked responses in the lower brainstem.
Kumar_A1; Tandon OP; Bhattacharya A; Gupta RK; Dhar D (1995) Somatosensory evoked potential changes after EAP therapy in chronic pain patients. Anaesthesia May 50(5):411-414. Dept of Anaesthesiology and Critical Care and Physiology, Univ Coll of Med Sci, Delhi, India. SEPs were recorded in 20 healthy volunteers and 20 patients with chronic pain undergoing EAP therapy. The values of absolute peak latency and amplitudes of N19 and P22 in the control group were compared with the corresponding baseline values in the study group and after EAP therapy at 3 stages during a 10-treatment cycle. On these occasions the intensity of pain was recorded using a 100 mm visual analogue scale score. Each patient in the study group had 10 treatments given every 2 d. The absolute peak latency of N19 was significantly delayed (p<.05) and reverted completely to control values after the 10th treatment (p>0.05). Visual analogue scores also decreased significantly. The neural mechanisms of EAP involve thalamic generation of SEPs, i.e. N19.
Lagerweij E; Nelis PC; Wiegant VM; van Ree JM (1984) The twitch in horses: a variant of AP. Science 14 Sept 225(4667):1172-1174.
Levin_MF; Hui Chan CW (1993) Conventional and AP-like TENS excite similar afferent fibres. Arch Phys Med Rehab Jan 74(1):54-60. Sch of Physical and Occupational Therapy, Faculty of Med, McGill Univ, Montreal, Quebec, Canada. The purpose of our study was to determine whether similar or different peripheral afferent fibre(s) is(are) activated by "conventional" TENS at low intensity-high frequency, as opposed to "AP-like" TENS at high intensity-low frequency. The electrostimulation was delivered to the median nerve at the wrist of 17 healthy subjects. For conventional TENS, single pulses were applied at an intensity of 3 X T (sensory threshold). Two kinds of AP-like TENS were studied: single pulses at 0.1Hz, and trains of 100Hz pulses at 4Hz, both delivered at an intensity greater than 3 X T. 30 compound action potentials/type of stimulation were recorded over the median nerve in the cubital fossa and averaged. Mean conduction velocities of the afferent fibres excited by conventional TENS, single pulse, and short-train AP-like TENS ranged from 50.3-65.4, 50.0-63.5, and 41.3-54.8m/s, respectively. Thus, conventional and AP-like TENS activated similar fibre types, mainly in the A alpha beta range. The effects of these two types of TENS may be mediated by the activation of similar peripheral afferent fibres.
Li_C; Zhu L; Li W; Ji C (1993) [Relationship between the presynaptic depolarization effect of AP and GABA, opioid peptide and Substance-P]. Chen Tzu Yen Chiu 18(3):178-182. Inst of AP, China Acad of TCM, Beijing, PRC. The present study was performed on 22 cats to explore whether GABA, endogenous opioid peptide and Substance-P (SP) were involved in the regulation of presynaptic inhibition in APA. The size of the antidromic compound C action potentials of the sural nerve evoked by the testing stimulation in spinal cord was measured as an indicator of C-afferent terminal excitability. It was found that EAP at GB30 and GB34 induced significant enlargement of the antidromic C-waves, showing the depolarization of presynaptic terminals of primary C-afferents was enhanced. The depolarization effect of EAP was significantly reduced by bicuculline, naloxone and the antiserum of SP locally applied to the surface of spinal cord respectively. It is supposed that GABA, endogenous opioid peptide and SP may be involved in the regulation of presynaptic inhibition in APA.
Li_KY; Zhu JM; Cao XD (1990) Effects of destruction of preoptic catecholaminergic nerve terminal on APA. Dept of Neurobiol, Shanghai Med Univ, PRC. AETRIJ 15(3-4):179-184. The present work studied the effect of preoptic catecholamine on APA. Catecholaminergic terminals were destroyed by microinjection of 6-hydroxydopamine into the preoptic area and the destruction was checked by fluorescence histochemical method. Destruction of catecholaminergic terminals significantly enhanced APA, suggesting that reduction of catecholamine level in the preoptic area may enhance APA.
Liu_C; Zhao F; Zhu L (1994) [Involvement of purines in analgesia produced by weak EAP]. Chen Tzu Yen Chiu 19(1):59-62, 54. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. In the present investigation the intensity of stimulated EAP (EA) was measured by electrophysiological collision technique. In the behavioral experiments, weak EAP at GB34 and GB39 (50 Hz, 1-1.5mA, not enough to activated A delta afferent fibres), prolonged the latency of nociceptive hind limb withdrawal reflex, but not the ail-flick latency. Both ip theophylline and caffeine (P1-purinergic (adenosine) receptor antagonists) blocked EAP-induced elevation of nociceptive thresholds in a dose-effect related manner, whereas dipyridamole (an inhibitor of adenosine release) shortened the after-effect of EAP in a dose dependent way. Weak EAP may induce analgesia and purines appear to be involved in this process.
Liu_C1; Zhao F; Li W; Zhu L (1994) Role of adenosine in weak EAP-induced depression of nociceptive response of spinal dorsal horn neurons in rats. Chen Tzu Yen Chiu - AP Research 19(2):52-55. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. Extracellular recordings were made from wide dynamic range (WDR) neurons in lumbar segments of the spinal cord in rats transected at the first lumbar segment. The nociceptive discharges of WDR neurons were depressed by weak EAP at GB34 and GB39. The depression was blocked by adenosine receptor antagonists, theophylline and caffeine iv. Depression of the nociceptive response of the WDR neurons induced by weak EAP may be mediated by adenosine within the spinal cord.
Liu_JL; Han XW; Su SN (1990) The role of frontal neurons in pain and APA. Sci China [B] Aug 33(8):938-945. Inst of Space Medico-Engineering, Beijing, PRC. To study the role of frontal neurons in pain and APA, experiments were carried out on 4 monkeys (Macaca mulatta) during performing 2 tasks, the Heat Discrimination Response GO/NO-GO Task (Task I) and the Heat Delayed Discrimination GO/NO-GO Task (Task II). After a criterion of 90% of correct performances over 3 d consecutively had been reached, activity of single neurons was recorded from the frontal cortex. Of 276 Task I-related neurons, 211 responded to noxious and/or innocuous heat stimuli. Of 73 Task II-related neurons, 59 responded to noxious and/or innocuous heat stimuli. During AP, the nociceptive reaction time for lever release to avoid painful stimuli was increased, the % of correct performances was lowered, and the neuronal responses to noxious and/or innocuous stimuli were suppressed. These neurons were mainly located in a circumscribed area medial to the superior ramus of the arcuate sulcus in frontal cortex, including the prefrontal and premotor areas. It is suggested that neurons in this area may be related to the discrimination of noxious and innocuous stimuli. The suppression of the activity of these neurons during AP may be involved in the whole mechanism of AP to facilitate the production of analgesia.
Liu_M; Liu X; Liu B (1991) [The analgesic effect of red nucleus and strengthening effect thereof to the APA]. Chen Tzu Yen Chiu 16(1):48-53. Dept of Physiol, N. Bethune Univ of Med Sciences, Changchun, PRC. The modulation of red nucleus (RN) to pain sense was researched with the latent period of radiant-heat tail flick of rats as the standard of the pain threshold. Bilateral injection of glutamic acid into RN significantly raised the pain threshold of tail flick reflex. Simultaneous injection of glutamic acid into RN and lidocaine into nucleus raphe magnus (NRM) attenuated that effect. The activated RN has analgesic effect and the NRM plays an important role in the descending inhibitory pathway of RN. The discharges of neurons in caudal part of nucleus spinalis tract nervi trigemini (cNST) evoked by stimulating nerve alveolaris inferior (nAI) with strong pulse were recorded with microelectrode. nAI-evoked discharges were inhibited by stimulating contralateral or ipsilateral RN. The RN inhibitory time course on nAI-evoked discharges were shortened after injecting lidocaine into NRM. The inhibitory effect of RN on neurons in cNST is mediated by NRM. EAP at ST06 inhibited the pain-evoked discharges of neurons in cNST. The time of EAP analgesia was prolonged by stimulating the RN. Activation of the RN enhances APA.
Liu_W; Song C; Yang J; Lin B; Wang C (1990) [Involvement of oxytocin in spinal cord in APA]. Chen Tzu Yen Chiu 15(1):24-29. Dept of Neurobiol, 2nd Military Coll, Shanghai, PRC. The influence of i.t. injection of oxytocin (OT), anti-OT serum (AOTS) and naloxone on pain threshold and EAP (EA) analgesia in rats was investigated. The tail-flick induced by potassium iontophoresis was used to measure the pain threshold. The increase in pain threshold was observed within 70 min after OT injection (100 ng), and it was much more effective than that of the ACSF injection (p <.001). OT administration enhanced EAP analgesia. This effect was dose-related. Although injection of AOTS did not affect the pain threshold, it diminished EAP analgesia. Also, injection of naloxone did not influence the action of OT on EAP analgesia. OT in the spinal cord is important in EAP analgesia, and its effects are independent of endogenous opiate peptides.