• The Korean Journal of Physiology
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• v.29 no.2
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• pp.309-321
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• 1995

In the present study, the relationship between the somatosympathetic reflexes and arterial blood pressure responses to electrical stimulation of the peripheral nerve was investigated in cats anesthetized with ${\alpha}-chloralose$. Single sympathetic postganglionic fiber activities were recorded from the hindlimb muscle and skin nerves and also from the cervical and abdominal sympathetic chains. Effects of the morphine on responses of the sympathetic nerve and arterial blood pressure to activation of the peripheral $A{\delta}-$ and C-afferent nerves were analyzed. The following results were obtained. 1) Arterial blood pressure was depressed by peripheral AS-afferent stimulation (A-response) and was elevated during C-afferent activation (C-response). 2) Intravenously administered morphine enhanced the C-response while the A-response decreased insignificantly, Only the C-response was decreased by intrathecal morphine. 3) All the ten recorded cutaneous sympathetic fibers showed periodic discharge pattern similar to respiratory rhythm and five of them also showed cardiac-related rhythm. However, most of the muscular sympathetic fibers had cardiac-related rhythm and only four fibers showed respiratory rhythm. 4) Morphine decreased the sympathetic C-reflex elicited by the peripheral C-afferent activation and the abdominal sympathetic A-reflex was also decreased by morphine. From the above results, it was concluded that supraspinal mechanisms were involved in the enhanced arterial pressor response to peripheral C-afferent activation by intravenous morphine.

• The Journal of Korean Medicine
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• v.26 no.3 s.63
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• pp.239-248
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• 2005

Objectives : Electroacupuncture (EA)-induced analgesia has been known to be mediated through the activation of opioid, noradrenergic and serotonergic receptors. However, little study on serotonergic mechanism has been performed in an animal model of chronic pain. The present study was designed to elucidate the type of serotonergic receptors responsible for EA analgesia in the chronic pain model. Methods : In rats with complete Freund's: adjuvant-induced inflammation and spinal nerve injury, spinal wide dynamic range (WDR) cell responses to graded electrical stimulation of afferent C fiber were recorded before and after spinal application of selective 5-hydroxytryptamine (5-HT) receptor antagonists. EA stimulation (2Hz, 0.5msec, 3mA) was applied to the contralateral Zusanli point for 30 min. Results : In both models of chronic pain, WDR cell responses were greatly inhibited after EA stimulation. EA-induced inhibition of WDR celt responses was significantly attenuated by spinal application of non-selective 5-HT receptor antagonist, dihydroergocristine Of 5-HT receptor antagonists tested, 5-HT1A (WAY 100635) and 5-HT2 (LY53857) receptor antagonists strongly reduced an ability of EA stimulation to inhibit WDR cell responses. However, 5-HT1B (GR55562) and 5-HT3 (LY278584) receptor antagonists also had weak but significant blocking action on EA-induced inhibitory effect on chronic pain. Conclusions : Dorsal hem cell responses, afferent C fiber stimulation, chronic pain, electroacupuncture, serotonergic receptors.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.108-117
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• 2003

Objective : The central opioid mechanism of acupuncture analgesia has been fairly well documented in acute behavioral experiments, but little electrophysiological study has been performed on the peripheral mechanism and subtypes of opioid receptors responsible for acupuncture-induced antinociception in chronic animal models. In the present electrophysiological experiment, we studied the peripheral mechanism and opioid receptor subtypes which Were implicated in electroacupuncture-induced antinociception in the rat with chronic inflammatory and neurogenic pain. Methods : In the rat with complete Freund's adjuvant-induced inflammation and spinal nerve injury, dorsal horn cell responses to afferent C fiber stimulation were recorded before and after electroacupuncture (EA) stimulation applied to the contralateral Zusanli point for 30 minutes. Also studied Were the effects of specific opioid receptor antagonists and naloxone methiodide, which can not cross the blood-brain barrier, on EA-induced inhibitory action. Results : EA-induced inhibitory action was significantly attenuated by naloxone methiodide, suggesting that EA-induced inhibition was mediated through peripheral mechanism. Pretreatment, but not posttreatment of naltrexone and spinal application significantly blocked EA-induced inhibitory actions. In inflammatory and neurogenic pain models, ${\mu}-$ and ${\delta}-opioid$ receptor antagonists (${\beta}-funaltrexamine$ & naltrindole) significantly reduced EA-induced inhibitory action, but ${\kappa}-opioid$ receptor antagonist had weak inhibitory effect on EA-induced antinociception. Conclusion : These results suggest that 2Hz EA-stimulation induced antinoeiceptive action is mediated through peripheral as well as central mechanism, and mainly through ${\mu}-$ and ${\delta}-opioid$ receptors.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.625-637
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• 1997

Calcium ions are implicated in a variety of physiological functions, including enzyme activity, membrane excitability, neurotransmitter release, and synaptic transmission, etc. Calcium antagonists have been known to be effective for the treatment of exertional angina and essential hypertension. Selective and nonselective voltage-dependent calcium channel blockers also have inhibitory action on the acute and tonic pain behaviors resulting from thermal stimulation, subcutaneous formalin injection and nerve injury. This study was undertaken to investigate the effects of iontophoretically applied $Ca^{++}$ and its antagonists on the responses of WDR (wide dynamic range) cells to sensory inputs. The responses of WDR cells to graded electrical stimulation of the afferent nerve and also to thermal stimulation of the receptive field were recorded before and after iontophoretical application of $Ca^{++}$, EGTA, $Mn^{++}$, verapamil, ${\omega}-conotoxin$ GVIA, ${\omega}-conotoxin$ MVIIC and ${\omega}-agatoxin$ IVA. Also studied were the effects of a few calcium antagonists on the C-fiber responses of WDR cells sensitized by subcutaneous injection of mustard oil (10%). Calcium ions and calcium channel antagonists ($Mn^{++}$, verapamil, ${\omega}-conotoxin$ GVIA & ${\omega}-agatoxin$ IVA) current-dependently suppressed the C-fiber responses of WDR cells without any significant effects on the A-fiber responses. But ${\omega}-conotoxin$ MVIIC did not have any inhibitory actions on the responses of WDR cell to A-fiber, C-fiber and thermal stimulation. Iontophoretically applied EGTA augmented the WDR cell responses to C-fiber and thermal stimulations while spinal application of EGTA for about $20{\sim}30\;min$ strongly inhibited the C-fiber responses. The augmenting and the inhibitory actions of EGTA were blocked by calcium ions. The WDR cell responses to thermal stimulation of the receptive field were reduced by iontophoretical application of $Ca^{++}$, verapamil, ${\omega}-agatoxin$ IVA, and ${\omega}-conotoxin$ GVIA but not by ${\omega}-conotoxin$ MVIIC. The responses of WDR cells to C-fiber stimulation were augmented after subcutaneous injection of mustard oil (10%, 0.15 ml) into the receptive field and these sensitized C-fiber responses were strongly suppressed by iontophoretically applied $Ca^{++}$, verapamil, ${\omega}-conotoxin$ GVIA and ${\omega}-agatoxin$ IVA. These experimental findings suggest that in the rat spinal cord, L-, N-, and P-type, but not Q-type, voltage-sensitive calcium channels are implicated in the calcium antagonist-induced inhibition of the normal and the sensitized responses of WDR cells to C-fiber and thermal stimulation, and that the suppressive effect of calcium and augmenting action of EGTA on WDR cell responses are due to changes in excitability of the cell.

• Journal of Acupuncture Research
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• v.19 no.4
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• pp.167-182
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• 2002

This experiment was designed to investigate the effects of electroacupuncture (EA) on chronic pains and factors that affected EA effects. The responses of wide dynamic range (WDR) cells to electrical stimulation of $A{\delta}$ & C afferent fibers were used as an index of pain in rats with chronic pains induced by intraplantar injection of complete Freund's adjuvant or peripheral nerve injury. In rats with chronic pains, low (2Hz) and high (100Hz) frequency EA stimulation applied to zusanli caused the inhibition of WDR cell responses in about 60% of rats and the inhibitory actions were dependent on the stimulus strength. EA stimulation also induced an excitation of WDR cell responses in 23.9% of rats and no effect in 15.8% of rats. However, it seemed that in normal rats compared to the rat with chronic pains, the incidence of which EA stimulation caused the excitation or no effect was high. Reversible spinalization almost completely blocked EA-induced inhibitory or excitatory effects. EA stimulation more frequently induced the excitation of WDR cell responses in lightly anesthetized (0.6%) rats and the enhanced responses of WDR cells were inhibited by EA stimulation in the rat anesthetized with 1.5% enflurane. These experimental findings suggest that in rats with chronic pain, EA stimulation inhibited WDR cell responses to slow $A{\delta}$ and C fiber stimulation and EA-induced inhibitory action was under the control of descending inhibitory system and degree of anesthesia.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.6
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• pp.661-670
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• 1998

Dopamine has been generally known to exert antinociceptive action in behavioral pain test, such as tail flick and hot plate test, but there appears to be a great variance in the reports on the antinociceptive effect of dopamine depending on the dosage and route of drug administration and type of animal preparation. In the present study, the effects of dopamine on the responses of wide dynamic range (WDR) cells to mechanical, thermal and graded electrical stimuli were investigated, and the dopamine-induced changes in WDR cell responses were compared between animals with an intact spinal cord and the spinal animals. Spinal application of dopamine (1.3 & 2.6 mM) produced a dose-dependent inhibiton of WDR cell responses to afferent inputs, the pinch-induced or the C-fiber evoked responses being more strongly depressed than the brush-induced or the A-fiber evoked responses. The dopamine-induced inhibition was more pronounced in the spinal cat than in the cat with intact spinal cord. The responses of WDR cell to thermal stimulation were also strongly inhibited. Dopamine $D_2$ receptor antagonist, sulpiride, but not $D_1$ receptor antagonist, significantly blocked the inhibitory action of dopamine on the C-fiber and thermal responses of dorsal horn cells. These findings suggest that dopamine strongly suppresses the responses of WDR cells to afferent signals mainly through spinal dopamine $D_2$ receptors and that spinal dopaminergic processes are under the tonic inhibitory action of the descending supraspinal pathways.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.3
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• pp.237-244
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• 1999

Magnesium ion is known to selectively block the N-methyl-D-aspartate (NMDA)-induced responses and to have anticonvulsive action, neuroprotective effect and antinociceptive action in the behavioral test. In this study, we investigated the effect of $Mg^{2+}$ on the responses of dorsal horn neurons to cutaneous thermal stimulation and graded electrical stimulation of afferent nerves as well as to excitatory amino acids and also elucidated whether the actions of $Ca^{2+}$ and $Mg^{2+}$ are additive or antagonistic. $Mg^{2+}$ suppressed the thermal and C-fiber responses of wide dynamic range (WDR) cell without any effect on the A-fiber responses. When $Mg^{2+}$ was directly applied onto the spinal cord, its inhibitory effect was dependent on the concentration of $Mg^{2+}$ and duration of application. The NMDA- and kainate-induced responses of WDR cell were suppressed by $Mg^{2+}$, the NMDA-induced responses being inhibited more strongly. $Ca^{2+}$ also inhibited the NMDA-induced responses current-dependently. Both inhibitory actions of $Mg^{2+}$ and $Ca^{2+}$ were additive, while $Mg^{2+}$ suppressed the EGTA-induced augmentation of WDR cell responses to NMDA and C-fiber stimulation. Magnesium had dual effects on the spontaneous activities of WDR cell. These experimental findings suggest that $Mg^{2+}$ is implicated in the modulation of pain in the rat spinal cord by inhibiting the responses of WDR cell to noxious stimuli more strongly than innocuous stimuli.

• The Korean Journal of Physiology
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• v.21 no.1
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• pp.59-66
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• 1987

This study was aimed to investigate whether the conduction velocity of nerve impulses through the ventral afferent fibers is constant along their entire courses in dorsal as well as in ventral roots. Cats were anesthetized with ${\alpha}-chloralose$ (60 mg/kg, i.p.) and artificially ventilated. Laminectomies were done on L4-S1 spinal vertebrae to expose the lumbosacral spiral cord. Both ventral and dorsal roots of L7 or S1 spinal segments were isolated and cut near the spinal cord. Ventral roots were placed on 6-lead stimulating electrodes and stimulated with supra C-threshold intensity. Divided dorsal root fascicles were placed on bipolar recording electrodes and single fiber units activated by the stimulation of the ventral roots were identified. Followings are the results obtained: 1) A total of 27 VRA units were identified. 10 units of them conducted impulses slower than 2 m/sec. Conduction velocities of the remaining units were in the range of 3.11-20.91 m/sec. 2) In 12 Units conduction velocities Of the VRA units through dorsal$(CV_{DR})$ and venral root$(CV_{DR})$ were determined respectively. There was a tendency to conduct impulses faster through dorsal roots$(CV_{DR}=8.19{\pm}3.26\;m/sec)$ than ventral roots$(CV_{DR}=3.46{\pm}1.02\;m/sec)$. From the above results we confirmed that there exist nerve fibers in continuity between the spinal ventral and dorsal roots but we could not ascertain whether there is a change in conduction velocity through the entire course of ventral afferent unit.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.113-122
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• 1994

The present study was carried out to characterize the functional properties of spinomesencephalic tract (SMT) neurons in the lumbar spinal cord of urethane anesthetized rats. Extracellular single unit recordings were made from neurons antidromically activated by stimulation of the midbrain area, including the deep layers of superior colliculus, periaqueductal gray and midbrain reticular formation. Recording sites were located in laminae I-VII of spinal cord segments of L2-L5. Receptive field properties and responses to calibrated mechanical stimulation were studied in 78 SMT cells. Mean conduction velocity of SMT neurons was $19.1{\pm}1.04\;m/sec$. SMT units were classified according to their response profiles into four groups: wide dynamic range (58%), deep/tap (23%), high threshold (9%) and low threshold (3%). A simple excitatory receptive field was found for most SMT neurons recorded in superficial dorsal horn (SDH). Large complex inhibitory and/or excitatory receptive fields were found for cells in lateral reticulated area which usually showed long after-discharge. Most of SMT cells received inputs from $A{\delta}$ and C afferent fiber types. These results suggest that sensory neurons in the rat SMT may have different functional roles according to their location in the spinal cord in integrating and processing sensory inputs including noxious mechanical stimuli.

• The Journal of Korean Medicine
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• v.25 no.3
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• pp.67-77
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• 2004

Objectives : Many studies have reported that acupuncture analgesia was mediated through the activation of peripheral and central opioid receptors. However, there has been little electrophysiological study on the adrenergic mechanism of acupuncture analgesia in chronic inflammatory and neuropathic pain. The present study was undertaken to elucidate the role of adrenoceptors in the production of acupuncture analgesia in the chronic pain model. Methods : In the rat with chronic inflammation and nerve injury, dorsal horn cell (DHC) responses to afferent C fiber stimulation were used as a pain index and changes in electroacupuncture (EA) analgesia were recorded before and after intravenous administration of selective adrenoceptor antagonists. EA stimulations (2Hz, 0.5msec, 3mA) were applied to the contralateral Zusanli point for 30 min. Results : EA stimulation induced long-lasting inhibition of DHC responses in the rat with chronic inflammation and nerve injury. In both models of inflammation and neuropathic pain, α-adrenoceptor antagonist (phentolamine) significantly attenuated an inhibitory effect of EA on DHC responses. Selective α2-adrenoceptor antagonist (yohimbine) also had a similar suppressive action on DHC responses to that of phentolamine. However, β-adrenoceptor antagonist (propranolol) did not have any inhibitory effect on DHC responses in either model of chronic pain. Conclusions : These experimental findings suggest that in rats with chronic pain, EA stimulation with low frequency and high intensity produced an analgesic effect which was mediated through an activation of α2-adrenoceptors.