ラット培養脊髄後根神経節ニューロンにおけるノルアドレナリンのブラジキニン応答への影響

―ホールセルパッチクランプ法による電気生理学的解析―

抄録

It is widely accepted that the sympathetic nerve activity might participate in some mechanisms underlying neuropathic pain which sometimes develops after nerve injuries.
Many chemical substances have been proposed to induce pain sensation. Bradykinin (BK) is the most potent in exciting nociceptors and in sensitizing them to thermal and mechanical stimuli. We investigated modulatory effects of sympathetic agents on BK actions in primary afferent dorsal root ganglion (DRG) cells. The present electrophysiological experiments by using the patch clamp technique were conducted to examine the effects of noradrenaline (NA) on BK responses and to determine the sites and mechanism of interaction between them.
1. Small (diameter, 20-35μum) DRG neurons responded to BK with inducing inward currents (BK-responses), but no BK responses could be evoked in DRG neurons larger than 35μm.
2 . NA at 10μM augmented the BK responses in amplitude compared to the control response.
3 . Clonidine at 1μM augmented the BK responses in amplitude, but isoproterenol at 1μM failed to augment the BK responses.
4. After pretreatment with yohimbine, the BK responses were not changed by NA.
It is concluded that NA-induced augmentation of the BK actions occurred by activating a 2-adrenergic receptor. Furthermore, this experimental system is a useful model in order to study the cellular mechanisms of neuropathic pain.