Effects of Munc13-1 and Munc18-1 on dopamine secretion dysfunction in manganese-exposed SH-SY5Y cells / 环境与职业医学

Background Neurotransmitter secretion disorder induced by chronic manganese poisoning has always been one of the important causes of body injury, but the mechanism of neurotransmitter secretion disorder caused by manganese is not clear at present. Objective To investigate the effects of presynaptic membrane intracellular protein 13-1 (Munc13-1) and synapse fusion protein binding protein 18-1 (Munc18-1) on dopamine secretion dysfunction induced by manganese chloride (MnCl2) in human neuroblastoma (SH-SY5Y) cells. Methods A SH-SY5Y cell model induced by MnCl2 was established. Cell viability was measured by MTT assay. Four experimental groups were set up: control group and low-, medium-, and high-dose manganese groups (0, 100, 200, and 400 μmol·L−1 MnCl2). They were treated with corresponding doses of MnCl2 for 24 h. The secretion of dopamine was measured by enzyme-linked immunosorbent assay. The mRNA expression of Syntaxin-1 was detected by real-time quantitaive PCR. Total cell proteins were extracted, and the protein expression levels of Munc13-1, Munc18-1, and Syntaxin-1 were detected by Western blotting. The correlations of MnCl2 exposure and dopamine secretion with the protein expressions of Munc13-1 and Munc18-1 were also analyzed by Pearson correlation. Results Compared with the control group, the cell viability rate decreased gradually with the increase of manganese exposure concentration, and the difference between the medium- and the high-dose manganese groups was statistically significant (P<0.05). The concentration of dopamine in cell culture medium of all manganese exposure groups decreased with the increase of manganese concentration, and compared with the control group and the low-dose manganese group, the medium- and the high-dose manganese groups were statistically significant (P<0.05). The expression of Syntaxin-1 at mRNA or protein level did not change significantly among groups (P>0.05). Compared with the control group, the protein expression of Munc13-1 decreased and that of Munc18-1 increased with the increase of manganese concentration (P<0.05). Compared with the low-dose manganese group, the changes of Munc13-1 protein in the high-dose manganese group and Munc18-1 protein in the medium- and high-dose manganese groups had statistical significance (P<0.05). Compared with the medium-dose manganese group, the protein changes of Munc18-1 in the high-dose manganese group were statistically significant (P<0.05). The correlation analysis showed that MnCl2 dose was negatively correlated with Munc13-1 protein expression (r=−0.898, P<0.05), and positively correlated with Munc18-1 protein expression (r=0.678, P<0.05). Dopamine secretion was positively correlated with Munc13-1 protein expression (r=0.932, P<0.05), and negatively correlated with Munc18-1 protein expression (r=−0.817, P<0.05). Conclusion The inhibition of dopamine secretion in SH-SY5Y cells induced by manganese exposure is related to up-regulation of Munc18-1 and down-regulation of Munc13-1 expression levels, which may be one of the reasons for nerve injury caused by manganese.

Interpretation of presynaptic dopaminergic PET imaging results / 中华核医学与分子影像杂志

Presynaptic dopaminergic PET imaging is a useful method for the diagnosis of parkinsonism. Based on the expert consensus on operation and clinical application of dopamine transporter brain PET imaging technology published in 2020, this paper further recommends the relevant elements of result interpretation of presynaptic dopaminergic PET imaging.

Methanolic extract of Rhinella schneideri (Anura: Bufonidae) poison causes ultrastructural changes in nerve terminals of phrenic nerve-diaphragm preparations in mice / Extracto metanólico de Rhinella schneideri (Anura: Bufonidae) causa cambios ultraestructurales en las terminaciones nerviosas de preparaciones de nervio frénico de ratón

Abstract Rhinella schneideri (or Bufo paracnemis), popularly known in Brazil as cururu toad, is also found in other countries in South America. The cardiovascular effects of this poison are largely known and recently was shown that it is capable to affect the neuromuscular junction on avian and mice isolated preparation. In this work, we used transmission electron microscopy to investigate the ultrastructure of the motor nerve terminal and postsynaptic junctional folds of phrenic nerve-hemidiaphragm preparations incubated for either 5 or 60 min with the methanolic extract of R. schneideri (50 µg/mL). In addition, the status of the acetylcholine receptors (AChR) was examined by TRITC-α-bungarotoxin immunofluorescence location at the endplate membrane. The results show that 5 min of incubation with the gland secretion extract significantly decreased (32 %) the number of synaptic vesicles into the motor nerve terminal, but did not decrease the electron density on the top of the junctional folds where nicotinic receptors are concentrated; however, 60 min of incubation led to significant nerve terminal reloading in synaptic vesicles whereas the AChR immunoreactivity was not as marked as in control and after 5 min incubation. Muscle fibers were well-preserved but intramuscular motor axons were not. The findings corroborated pharmacological data since the decrease in the number of synaptic vesicles (5 min) followed by recovery (60 min) is in accordance with the transient increase of MEPPs frequency meaning increased neurotransmitter release. These data support the predominant presynaptic mode of action of the R. schneideri, but do not exclude the possibility of a secondary postsynaptic action depending on the time the preparation is exposed to poison. Rev. Biol. Trop. 66(3): 1290-1297. Epub 2018 September 01.

Resumen Rhinella schneideri (o Bufo paracnemis), conocido popularmente en Brasil como sapo cururu, también se encuentra en otros países de América del Sur. Los efectos cardiovasculares de este veneno son ampliamente conocidos y recientemente se demostró que es capaz de afectar la unión neuromuscular en la preparación aislada de aves y ratones. En este trabajo, utilizamos microscopía electrónica de transmisión para investigar la ultraestructura de la terminación nerviosa motora y pliegues de unión postsináptica de preparaciones de nervio frénico-hemidiafragma incubadas durante 5 o 60 min con el extracto metanólico de R. schneideri (50 μg/mL). Además, se examinó el estado de los receptores de acetilcolina (AChR) mediante la ubicación de inmunofluorescencia de TRITC-α-bungarotoxina en la membrana de la placa terminal. Los resultados muestran que 5 min de incubación con el extracto de secreción de glándula disminuyeron significativamente (32 %) el número de vesículas sinápticas en el terminal del nervio motor, pero no disminuyeron la densidad electrónica en la parte superior de los pliegues de unión donde se concentran los receptores nicotínicos. Sin embargo, 60 min de incubación condujeron a una recarga significativa de los terminales nerviosos en las vesículas sinápticas, mientras que la inmunorreactividad del AChR no fue tan marcada como en el control y después de 5 min de incubación. Las fibras musculares estaban bien conservadas, pero los axones motores intramusculares no. Los hallazgos corroboraron los datos farmacológicos ya que la disminución en el número de vesículas sinápticas (5 min) seguida de recuperación (60 min) está de acuerdo con el aumento transitorio de la frecuencia de MEPPs, lo que significa una mayor liberación de neurotransmisores. Estos datos apoyan el modo de acción presináptico predominante de R. schneideri, pero no excluyen la posibilidad de una acción postsináptica secundaria dependiendo del tiempo en que la preparación esté expuesta al veneno.

Role of Pre-Synaptic NMDA Receptors in the Modulation of Inhibitory Synaptic Transmission in Sensory-Motor and Visual Cortical Pyramidal Neurons in Brain Slices of Young Epileptic Mice

Background: Previous studies from animal models have shown that pre-synapticNMDA receptors (preNMDARs) are present in the cortex, but the role of inhibition mediated bypreNMDARs during epileptogenesis remains unclear. In this study, we wanted to observe thechanges in GABAergic inhibition through preNMDARs in sensory-motor and visual corticalpyramidal neurons after pilocarpine-induced status epilepticus.Methods: Using a pilocarpine-induced epileptic mouse model, sensory-motor and visualcortical slices were prepared, and the whole-cell patch clamp technique was used to recordspontaneous inhibitory post-synaptic currents (sIPSCs).Results: The primary finding was that the mean amplitude of sIPSC from the sensorymotorcortex increased significantly in epileptic mice when the recording pipette contained MK-801 compared to control mice, whereas the mean sIPSC frequency was not significantly different,indicating that post-synaptic mechanisms are involved. However, there was no significant presynapticinhibition through preNMDARs in the acute brain slices from pilocarpine-inducedepileptic mice.Conclusion: In the acute case of epilepsy, a compensatory mechanism of post-synapticinhibition, possibly from ambient GABA, was observed through changes in the amplitude withoutsignificant changes in the frequency of sIPSC compared to control mice. The role of preNMDARmediatedinhibition in epileptogenesis during the chronic condition or in the juvenile stagewarrants further investigation.

Presynaptic neuromuscular action of a methanolic extract from the venom of Rhinella schneideri toad

Rhinella schneideri, previously known as Bufo paracnemis, is a common toad in many regions of Brazil. Its venom exerts important cardiovascular effects on humans and other animals. Although this toad venom has been the subject of intense investigations, little is known about its neuromuscular activity. The neurotoxicity of a methanolic extract of R. schneideri venom was tested on mouse phrenic nerve-diaphragm (PND) preparations mounted for conventional twitch tension recording – in response to indirect stimulation – and for electrophysiological measurements.

Presynaptic neuromuscular action of a methanolic extract from the venom of Rhinella schneideri toad

Rhinella schneideri, previously known as Bufo paracnemis, is a common toad in many regions of Brazil. Its venom exerts important cardiovascular effects on humans and other animals. Although this toad venom has been the subject of intense investigations, little is known about its neuromuscular activity. The neurotoxicity of a methanolic extract of R. schneideri venom was tested on mouse phrenic nerve-diaphragm (PND) preparations mounted for conventional twitch tension recording – in response to indirect stimulation – and for electrophysiological measurements.

Comparação de inibições medulares entre indivíduos com doença de Parkinson e saudáveis / Comparison of spinal inhibitions between parkisonian and helathy individuals

O objetivo do presente estudo foi comparar os níveis de inibição pré-sináptica (IPS) e inibição recíproca (IR) entre indivíduos com Doença de Parkinson e saudáveis e, a correlação entre essas inibições e a rigidez muscular e a severidade clínica de indivíduos com Doença de Parkinson (avaliadas através da Escala Unificada de Avaliação da Doença de Parkinson). Foram avaliados 11 indivíduos nos estágios 2 e 3 da doença e 13 indivíduos saudáveis pareados pela idade. A IPS foi menor em indivíduos com Doença de Parkinson (31,6%) do que em saudáveis (67,1%) (p = 0,02). A IR não diferiu entre indivíduos com Doença de Parkinson (26,9%) e saudáveis (27,6%) (p = 0,91). Adicionalmente, não foram detectadas correlações entre os níveis de IPS com a rigidez e a severidade clínica (p > 0,05). Portanto, mecanismos inibitórios não explicam totalmente a rigidez muscular e a severidade clinica da doença. Alterações entre ativação de músculos agonistas e antagonistas parecem estar relacionadas a influências supraespinhais anormais nos mecanismos espinhais decorrentes da doença...

The purposes of the present study were to compare presynaptic inhibition (PI) and disynaptic reciprocal inhibition (DRI) levels between parkinsonians and healthy individuals and to verify the correlation of such inhibitions with muscle rigidity and clinical severity (assessed by the Unified Parkinson Disease Rating Scale). We evaluated 11 parkinsonians in stages 2 and 3 of the disease and 13 healthy individuals matched for age. The PI was significant lower in parkinsonians (31.6%) than in healthy individuals (67.1%) (p = 0.02). The DRI did not differ between parkinsonians (26.9%) and healthy individuals (27.6%) (p = 0.91). Furthermore, no significant correlation was observed between PI with muscle rigidity and clinical severity (p > 0.05). Therefore, inhibitory mechanisms do not fully explain the cause of muscle rigidity and clinical severity of parkinsonians. Changes between the activation of agonist and antagonist muscles seem to be caused by abnormal supraspinal influence on spinal mechanisms...

Changes of Cochlear Nerve Terminals after Temporary Noise-Induced Hearing Loss / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Overexposure to intense sound can cause temporary or permanent hearing loss. Post-exposure recovery of thresholds has been assumed to indicate reversal of damage to the inner ear without persistent consequences for auditory function. However, there was a report that acoustic overexposures causing moderate temporary threshold shift caused acute loss of afferent nerve terminals and delayed degeneration of the cochlear ganglion cells while cochlear sensory cells were intact. The purpose of the study was to evaluate the numerical changes of ribbon synapses and efferents to the outer hair cells in ears with temporary noise-induced threshold shifts. MATERIALS AND METHODS: Four-week old CBA mice with normal Preyer's reflexes were used. Mice were exposed to white noise of 110 dB SPL for one hour. Auditory brainstem response (ABR) and distortion-product otoacoustic emission (DPOAE) were recorded before exposure and at four different post-exposure times, 1, 3, 5, and 7 days after noise exposure. Ribbon synapses and efferents near cochlear nerve terminals were stained and calculated in the control group mice at two post-exposure times, 3 and 5 days after the exposure. RESULTS: In the noise-exposed ears, there was no loss of hair cells, in either inner hair cells or outer hair cells. ABR and DPOAE showed maximum threshold shifts after noise-exposure; they returned to the normal pre-exposure values by at day 5. The number of ribbon synapses tended to decrease at 3 days after noise-exposure, but the number of efferent fibers was not statistically different from those of the control mice. CONCLUSION: Our results suggest that the loss of ribbon synapses could be related with the recovery course of temporary threshold shift, even to the point of full hearing recovery.

Neuromuscular activity of Bothrops neuwiedi pauloensis snake venom in mouse nerve-muscle preparations

The pharmacological effects of Bothrops neuwiedi pauloensis venom on mouse phrenic nerve-diaphragm (PND) preparations were studied. Venom (20 mug/ml) irreversibly inhibited indirectly evoked twitches in PND preparations (60 ± 10 percent inhibition, mean ± SEM; p<0.05; n=6). At 50 mug/ml, the venom blocked indirectly and directly (curarized preparations) evoked twitches in mouse hemidiaphragms. In the absence of Ca2+, venom (50 mug/ml), produced partial blockade only after an 80 min incubation, which reached 40.3 ± 7.8 percent (p<0.05; n=3) after 120 min. Venom (20 mug/ml) increased (25 ± 2 percent, p< 0.05) the frequency of giant miniature end-plate potentials in 9 of 10 end-plates after 30 min and the number of miniature end-plate potentials which was maximum (562 ± 3 percent, p<0.05) after 120 min. During the same period, the resting membrane potential decreased from - 81 ± 1.4 mV to - 41.3 ± 3.6 mV 24 fibers; p<0.01; n=4) in the end-plate region and from - 77.4 ± 1.4 to -44.6 ± 3.9 mV (24 fibers; p<0.01; n=4) in regions distant from the end-plate. These results indicate that B. n. pauloensis venom acts primarily at presynaptic sites. They also suggest that enzymatic activity may be involved in this pharmacological action.(AU)

Roles of metabotropic glutamate receptors on excitatory synaptic transmission in rat trigeminal caudal neurons

Muscarine M2 Receptor-mediated Presynaptic Inhibition of GABAergic Transmission in Rat Meynert Neurons

Cholinergic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) by the activation of muscarine receptors was investigated in mechanically dissociated rat nucleus basalis of the Meynert neurons using the conventional whole-cell patch recording configuration. Muscarine (10microM) reversibly and concentration-dependently decreased mIPSC frequency without affecting the current amplitude distribution. Muscarine action on GABAergic mIPSCs was completely blocked by 1microM methoctramine, a selective M2 receptor antagonist, but not by 1microM pirenzepine, a selective M1 receptor antagonist. NEM (10microM), a G-protein uncoupler, attenuated the inhibitory action of muscarine on GABAergic mIPSC frequency. Muscarine still could decrease GABAergic mIPSC frequency even in the Ca2+-free external solution. However, the inhibitory action of muscarine on GABAergic mIPSCs was completely occluded in the presence of forskolin. The results suggest that muscarine acts presynaptically and reduces the probability of spontaneous GABA release, and that such muscarine-induced inhibitory action seems to be mediated by G-protein-coupled M2 receptors, via the reduction of cAMP production. Accordingly, M2 receptor-mediated disinhibition of nBM neurons might play one of important roles in the regulation of cholinergic outputs from nBM neurons as well as the excitability of nBM neurons themselves.

Effects and mechanism of PNS on synaptic transmission in hippocampal CA1 region of rat / 中草药

Objective To investigate the effects of Panax notoginseng saponins(PNS)on both the excitatory and inhibitory synaptic transmission in the pyramidal neurons in hippocampal CA1 region of rats.Methods Wistar male rats(3—4 weeks)were killed by cervical dislocation and hippocampal slices(400 ?m)were prepared,blind whole-cell voltage-clamp recordings were performed on the CA1 pyramidal cells in hippocampal slices to examine and analyze the effects of PNS(0.05—0.4 g/L)on CA1 afferent fiber-evoked excitatory postsynaptic currents(EPSCs)and inhibitory postsynaptic currents(IPSCs),respectively.Moreover,the Schaffer collateral/commissural pathway was stimulated with paired pulses(interpulse interval was 50 ms)and the paired-pulse facilitation(PPF)was analyzed by EPSC2/EPSC1(P2/P1)ratio.Results PNS(0.1—0.4 g/L)significantly depressed amplitude of EPSCs in neurons in the hippocampal CA1 region(P0.05).Conclusion The inhibitory effect of PNS on EPSCs in hippocampal CA1 pyramidal neurons is not due to the reinforcement of the inhibiting interneurons.It may be a result of direct inhibition on excitatory synaptic transmission.The increasing of P2/P1 ratio after PNS application suggests that PNS depresses the excitatory synaptic transmission by presynaptic mechanism.

Effect of GABA on the contratility of small intestine isolated from rat / 영남의대학술지

This study was designed to investigate the effect of GABA and related substances on the spontaneous contraction of rat small intestine. The rats (Sprague-Dawley), weighing 200-250g, were sacrificed by cervical dislocation, and the small intestine was isolated. Longitudinal muscle strips from duodenum, jejunum and ileum were suspended in Biancani's isolated muscle chambers and myographied isometrically. GABA and muscimol, a GABA A receptor agonist relaxed the duodenum and jejunum significantly, but baclofen-induced relaxation in those muscle strips negligible. The effectiveness of GABA and muscimol in various regions were the greatest on duodenum, and greater on jejunum than on ileum The effect of GABA and muscimol was antagonized by bicuculline, a competitive GABA A receptor antagonist and picrotoxin, a noncompetitive GABA A receptor antagonist. Duodenal relaxation induced by GABA and muscimol was unaffected by hexamethonium, but was prevented by tetrodotoxin. These results suggest that GABA inhibit the contractility of smooth muscle with distinct regional difference of efficacy, and the site of inhibitory action is the GABA A receptor existing at the presynaptic membrane of postganglionic excitatory nerves.

Interactions of nicotinic and muscarinic acetylcholine receptors / 中国药理学通报

Nicotinic and muscarinic acetylcholine receptors have the same endogenous ligand ACh and are distributed together in many tissues, so it is reasonable to believe that there must be some interactions existed between them. The functions of muscarinic receptors in the tissues innervated by the parasympathetic cholinergic postfibers, can be modulated by the ganglionic nicotinic receptors through stimulating ACh release. In ganglia, the postsynaptic nicotinic receptor activities can be modulated by the presynaptic muscarinic and nicotinic autoreceptors through regulating ACh release. Moreover, The functions of muscarinic receptors can be changed by nicotinic receptor desensitization or blockade. The two types of receptor act on each other and keep in a varied homeostasis of cholinergic nervous system.

Imidazoline binding sites and receptors related with cardiovascular functions / 中国药理学通报

I 2 Imidazoline binding sites have been shown to exist on cardiac myocytes of human beings and rat. Both of I 1 and I 2 imidazoline binding sites have been identified on vascular smooth muscle cells of various species. Vascular I 2 imidazoline binding sites may participate in vascular smooth muscle proliferation. The sympathetic nerves supplying the cardiovascular system are endowed with presynaptic inhibitory imidazoline receptors. Being different from most of the imidazolines, moxonidine does not activate presynaptic imidazoline receptors, but SR141716A, which is considered as a selective antagonist at cannabinoid receptors, antagonizes presynaptic imidazoline receptors. It has been shown that imidazolines exhibit antiarrhythmic action. Agamatine, which is endogenous ligand at imidazoline receptors, not only decreases the rate of pacemaker firing in sinoatrial node of animal, prolongs action potential duration on cardiac myocytes of human beings and animal, but also inhibits afterdepolarizations induced by isoproterenol. On the other hand, imidazolines and guanidines inhibit the cardiovascular K ATP channel in a noncompetitive manner, those effects might interfere with the cardioprotective effects of K ATP channel.

Effect of GABA_B receports on taurine-regulate release of amino acids from rat cortical synaptosomes / 中国药理学通报

AIM Taurine can regulate Asp、 Glu、 GABA from rat cortical synaptosomes. But its mechanism is unclear. The release regulated effects were investigated through analysis of GABA receptors.METHODS Bicuculline、Phaclofen、Baclofen were added in a Krebs Ringer buffer with resuspended synapotomes.Endogenous Asp、 Glu and GABA release during the 5 min superfusion were measured by high perfusion liquid chromatography using percolumn durivatization with Dans Cl. RESULT Phaclofen,but not bicucullion baclofen, counteracted the inhibition of GABA overflow,although the inhibition of Asp and Glu overflow was not attenuated. CONCLUSION Taurine inhibits the depolarization evoked release of GABA through the activation of presynaptic autoreceptors and taurine also acts on presynaptic sits of Asp Glu nerve terminals to inhibit their evoked release in rat cerebral cotex.

THE INHIBITORY EFFECT OF STIMULATION IN PERIAQUEDUCTAL GREY ON NEURONS IN SPINAL DORSAL HORN AND ITS RELATION TO PAG-CDP / 西安交通大学学报(医学版)

The cord dorsum potential evoked by stimulation in the ventrolateral aspect of periaqueductal grey (PAG-CDP) was recorded from the dorsal surface of the spinal lumbosacral cord in rats. PAG stimulation with the same parameters as for producing PAG-CDP inhibited the C discharges of convergent neurons in spinal dorsal horn. There was a positive correlation between the time course of the inhibitory effect of PAG on convergent neurons and the duration of the slow wave of PAG-CDP. a positive correlation also presented between the latencies of the PAG inhibition and the slow wave. Furthermore, the PAG inhibition did not appear when the intensity of PAG stimulation was below the threshold of PAG-CDP. These results indicate that the presynaptic inhibition is involved in the PAG inhibition of the C discharges of convergent neurons in spinal dorsal horn.

INFLUENCES OF CONDITIONING STIMULI OF PERIPHERAL NERVE ON C-FIBRE AFFERENT TERMINAL EXCITABILITY IN SPINAL TOADS / 西安交通大学学报(医学版)

The antidromic C waves elicited by stimulating the entry zone of the dorsal root were recorded in spinal toads. Influences if conditioning stimuli in 60 T from sciatic nerve on antidromic C waves were observed. The conditioning stimuli produced marked increace in the excitability of the C-afferent terminals. The increased excitability possessed two phases. The results indicat that periphiral primary afferent A and C-fibres can produce presynaptic inhibition in C-fibre terminals.

Structure of presynaptic toxins: Crystallization and preliminary x-ray diffraction data on Notechis II-5, a presynaptic toxin phospholipase.

The presynaptic neutrotoxin-phospholipase, Notechis II-5 from the venom of Notechis Scutatus scutatus (Australian tiger snake) has been crystallized in a form suited for xray diffraction analysis. The crystals belong to the orthorhombic space group P21 21,21, with unit cell dimensions, a=146.1, b =43.5 and c=39.0 A. There are two molecules of Notechis II- 5 in the asymmetric unit. The molecular weight is about 13,500. Notechis II-5 is highly homologous to Notexin, another presynaptic toxin from the venom of the Australian tiger snake, to bovine and porcine pancreatic phospholipases A and other venom phospholipases.

THE EFFECT OF REMOTE SEGMENTAL ELECTRO-ACUPUNCTURE ON THE FLEXION REFLEX POTENTIAL AND THE DORSAL ROOT POTENTIAL / 西安交通大学学报(医学版)

Deseription was given of the effect of electric acupuncture of Neiguan point on the flexion reflex potential (FRP) of the hindlimbs and the dorsal root potential (DRP). On the intact and awake rats, the graded train stimulation (three pulses, 5ms interval, 0.5ms duration) was given to the sural nerve (a pure cutancous n(?), the C-FRP and C-DRP with their proper amplitudes (70～80% maximum) were obtained on the hamstring nerve (a group of nerves innervating the hindlimb flexors) and L5 dorsal root respectively. Then the electric acupuncture with low freqency and low intensity (4Hz, 1～3V)and low freqency and high intensity ( 4Hz, 20～40V), lasting 5 minutes, was given to the ipsilateral Neiguan point. After acupuncture, the amplitudes of both C-FRP and C-DRP decreased without change of their latebcues. The former one declined heavier and recovered slower than the latter one did. The A-FRP and A-DRP were not affected. Te result of the experiment suggests that the ipsilatcral Neiguan point cletric acupuncture can induce hindlimb's analgesia, the presynaptic inhibition might be involved in the mechanism of such analgesia.