• 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 Pain
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• v.12 no.2
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• pp.177-182
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• 1999

Background: Clonidine, an ${\alpha}_2$ adrenergic agonist blocks nerve conduction. However, in our previous experiment we found that adrenaline neither blocks nerve conduction by itself nor augment nerve conduction blockade by lidocaine near clinical concentrations. Possible explanations are: 1) there may be antagonism between some of adrenergic receptors, 2) clonidine may block nerve conduction via non-adrenergic mechanism. The purpose of this study is to obtain dose-response curves of several different forms of adrenergic receptor agonist to see the relative potencies of each adrenergic receptors to block nerve conduction. Methods: Recordings of compound action potentials of A-fiber components (A-CAPs) were obtained from isolated sciatic nerves of adult male Sprague-Dawley rats. Nerve sheath of the sciatic nerve was removed and desheathed nerve bundle was mounted on a recording chamber. Single pulse stimuli (0.5 msec, supramaximal stimuli) were repeatedly applied (2Hz) to one end of the nerve and recordings of A-CAPs were made on the other end of the nerve. Dose-response curves of epinephrine, phenylephrine, isoproterenol, clonidine were obtained. Results: $ED_{50}$ of each adrenergic agonist was: $4.51\times10^{-2}$ M for epinephrine; phenylephrine, $7.74\times10^{-2}$ M; isoproterenol, $9.61\times10^{-2}$ M; clonidine, $1.57\times10^{-3}$ M. Conclusion: This study showed that only clonidine, ${\alpha}_2$ adrenergic agonist, showed some nerve blocking action while other adrenergic agonists showed similar poor degree of nerve blockade. This data suggest that non-effectiveness of epinephrine in blocking nerve conduction is not from the antagonism between adrenergic receptors.