Maruo Keishi, Yamamoto Hideyuki, Yamamoto Satoshi, Nagata Tetsu, Fujikawa Hirokazu, Kanno Takeshi, Yaguchi Takahiro, Maruo Soji, Yoshiya Shinichi, Nishizaki Tomoyuki
Department of Physiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan Department of Orthopedics, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan.
Pain. 2006 Jan;120(1-2):106-112. doi: 10.1016/j.pain.2005.10.016. Epub 2005 Dec 19.
The present study examined noradrenaline-induced modulation of ATP-evoked currents in dorsal root ganglion (DRG) neurons after sciatic nerve injury (transection). ATP (10 microM) generated fast/mixed type of whole-cell membrane currents, possibly as mediated via P2X(3)/P2X(3)-like receptors, and slow type of the currents, possibly as mediated via P2X(2/3) receptors, in acutely dissociated L4/5 DRG neurons, without significant difference between sham and injury group. For sham group, noradrenaline (10 microM) enhanced fast/mixed type of ATP-evoked currents in ipsilateral DRG neurons, that is not inhibited by H-7, a broad inhibitor of protein kinases, but otherwise it had no effect on slow type of the currents. For injury group, noradrenaline (10 microM) significantly potentiated slow type of ATP-evoked currents in ipsilateral DRG neurons, that is abolished by H-7 or GF109203X, a selective inhibitor of protein kinase C (PKC), while it depressed fast/mixed type of the currents. In the analysis of real-time reverse transcription-polymerase chain reaction, an increase in the mRNAs for alpha(1b), alpha(2a), alpha(2d), and beta(2) adrenergic receptors was found with the ipsilateral DRGs after sciatic nerve injury. Collectively, the results of the present study suggest that noradrenaline potentiates P2X(2/3) receptor currents by activating PKC via alpha(1) adrenergic receptors linked to G(q) protein, perhaps dominantly alpha(1b) adrenergic receptors, in DRG neurons after sciatic nerve injury. This may account for a nociceptive pathway in response to noradrenergic sprouting after peripheral nerve injury.
本研究检测了坐骨神经损伤(横断)后,去甲肾上腺素对背根神经节(DRG)神经元中ATP诱发电流的调节作用。在急性分离的L4/5 DRG神经元中,ATP(10微摩尔)产生快速/混合型全细胞膜电流,可能是通过P2X(3)/P2X(3)样受体介导,以及慢速型电流,可能是通过P2X(2/3)受体介导,假手术组和损伤组之间无显著差异。对于假手术组,去甲肾上腺素(10微摩尔)增强了同侧DRG神经元中快速/混合型ATP诱发电流,这不受蛋白激酶广泛抑制剂H-7的抑制,但对慢速型电流无影响。对于损伤组,去甲肾上腺素(10微摩尔)显著增强了同侧DRG神经元中慢速型ATP诱发电流,这被H-7或蛋白激酶C(PKC)的选择性抑制剂GF109203X所消除,而它抑制了快速/混合型电流。在实时逆转录-聚合酶链反应分析中,发现坐骨神经损伤后同侧DRG中α(1b)、α(2a)、α(2d)和β(2)肾上腺素能受体的mRNA增加。总体而言,本研究结果表明,坐骨神经损伤后,去甲肾上腺素通过与G(q)蛋白偶联的α(1)肾上腺素能受体,可能主要是α(1b)肾上腺素能受体激活PKC,从而增强P2X(2/3)受体电流。这可能解释了外周神经损伤后对去甲肾上腺素能芽生的伤害性感受通路。