• The Korean Journal of Physiology
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• v.28 no.2
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• pp.123-132
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• 1994

The present study was undertaken to elucidate the desensitization of cutaneous receptors and the conduction block of the afferent nerves induced by direct application of allyl isotheocyanate (mustard oil) to the receptive field (RF) or onto the afferent nerve, respectively. Dorsal horn cell responses to mechanical stimulations of RF were completely suppressed when mustard oil was applied to either the afferent nerve or the whole area of RF. C-fiber responses of dorsal horn cells were more susceptive to mustard oil than A-fiber activities. This was confirmed by the experiment in which the compound action potentials recorded from rat tibial nerve before and after topical application of mustard oil were compared. The higher the concentration of mustard oil and the longer the application time, the more powerful desensitization or conduction block was induced. From the results of the present study, it is suggested that the desensitization of the afferent fiber and sensory receptors induced by mustard oil results mainly from the conduction block of C-fiber in the primary afferent nerve.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.5
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• pp.281-288
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• 2004

The present study was undertaken to confirm whether melittin, a major constituent of whole bee venom (WBV), had the ability to produce the same nociceptive responses as those induced by WBV. In the behavioral experiment, changes in mechanical threshold, flinching behaviors and paw thickness (edema) were measured after intraplantar (i.pl.) injection of WBV (0.1 mg & 0.3 mg/paw) and melittin (0.05 mg & 0.15 mg/paw), and intrathecal (i.t.) injection of melittin $(6{\mu}g)$. Also studied were the effects of i.p. (2 mg & 4 mg/kg), i.t. $(0.2{\mu}g\;&\;0.4{\mu}g)$ or i.pl. (0.3 mg) administration of morphine on melittin-induced pain responses. I.pl. injection of melittin at half the dosage of WBV strongly reduced mechanical threshold, and increased flinchings and paw thickness to a similar extent as those induced by WBV. Melittin- and WBV-induced flinchings and changes in mechanical threshold were dose- dependent and had a rapid onset. Paw thickness increased maximally about 1 hr after melittin and WBV treatment. Time-courses of nociceptive responses induced by melittin and WBV were very similar. Melittin-induced decreases in mechanical threshold and flinchings were suppressed by i.p., i.t. or i.pl. injection of morphine. I.t. administration of melittin $(6{\mu}g)$ reduced mechanical threshold of peripheral receptive field and induced flinching behaviors, but did not cause any increase in paw thickness. In the electrophysiological study, i.pl. injection of melittin increased discharge rates of dorsal horn neurons only with C fiber inputs from the peripheral receptive field, which were almost completely blocked by topical application of lidocaine to the sciatic nerve. These findings suggest that pain behaviors induced by WBV are mediated by melittin-induced activation of C afferent fiber, that the melittin-induced pain model is a very useful model for the study of pain, and that melittin-induced nociceptive responses are sensitive to the widely used analgesics, morphine.

• The Korean Journal of Physiology
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• v.26 no.2
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• pp.143-150
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• 1992

The purpose of this study is to obtain the effective concentration of capsaicin to relieve pain with no change in the number of C-fibers and its effective duration for pain relief. Capsaicin has been used extremely as a experimental tool and as topical medications for acute or chronic tissue injuries and partial nerve injury is the main cause of causalgiform pain disorders in humans. Here, the left sciatic nerve was ligated unilaterally at the high level of the thigh to prepare an animal model of this pain condition. The rat developed guarding behavior of the ipsilateral hind paw within a few hours after the operation and this behavior was maintained for several months thereafter, suggesting the possibility of spontaneous pain. These animals were divided into two groups(4-week & 8-week) and each group was subdivided into five groups by different concentration (0.05, 0.1, 0.5, 1.0 & 2.0%). Each capsaicin concentration was treated locally on the spinal cord-side of the ligated nerve and the foot withdrawal latency was measured. Thereafter, the dorsal roots of L5 were removed from both sides immediately after in tracardial perfusion for the counting of C-fibers by the histological procedure. There were no significant differences in the foot-withdrawal latency and the number of C-fibers between the left side treated with 0.05% capsaicin and the right side treated with the vehicle. However, latencies of the left sides treated with 0.1, 0.5, and 1.0% capsaicin increased significantly throughout 4-6 weeks with almost no change in the number of C-fibers, and the latencies showed the trends to approach slowly to those of the conditions after operation. The latency of subgroup treated with 2.0% increased by approximate 10% more than that of the right side throughout 8 weeks, and the number of C-fibers decreased by about 30% or more These results suggest that the elevated latency with capsaicin(0.1-1.0%) treatment is due to the inhibition of impulse transmission throughout the primary afferent fiber and the data from 2.0% are due to partial destruction of C-fibers. Therefore, capsaicin concentrations from 0.1% to 1.0% are probably very effective for the treatment of causalgiform pain with almost no destruction of C-fibers.

• International Journal of Oral Biology
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• v.34 no.4
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• pp.191-197
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• 2009

Somatostatin (SST) is a known neuromodulator of the central nervous system. The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives many thinmyelinated $A{\delta}$-fiber and unmyelinated C primary afferent fibers and is involved in nociceptive processing. Many studies have demonstrated that SST plays a pivotal role in pain modulation in the spinal cord. However, little is yet known about the direct effects of SST on the SG neurons of the Vc in adult mice. In our present study, we investigated the direct membrane effects of SST and a type 2 SST receptor agonist, seglitide (SEG), on the SG neurons of the Vc using a gramicidin-perforated current clamp in adult mice. The majority (53%, n = 27/51) of the adult SG neurons were hyperpolarized by SST (300 nM) but no differences were found in the hyperpolarization response rate between males and females. When SST was applied successively, the second response was smaller ($76{\pm}9.5%$, n=19), suggesting that SST receptors are desensitized by repeated application. SST-induced hyperpolarization was also maintained under conditions where presynaptic events were blocked ($75{\pm}1.0%$, n=5), suggesting that this neuromodulator exerts direct effects upon postsynaptic SG neurons. SEG was further found to induce membrane hyperpolarization of the SG neurons of the Vc. These results collectively demonstrate that SST inhibits the SG neuronal activities of the Vc in adult mice with no gender bias, and that these effects are mediated via a type 2 SST receptor, suggesting that this is a potential target for orofacial pain modulation.