Liu Zhen, Li Zhenzhong
Department of Anatomy, Shandong University School of Medicine, Jinan, Shandong Province 250012, People's Republic of China.
In Vitro Cell Dev Biol Anim. 2008 Sep-Oct;44(8-9):379-84. doi: 10.1007/s11626-008-9118-9. Epub 2008 Jun 14.
Galanin is a 29-amino-acid neuropeptide expressed in dorsal root ganglion (DRG) neurons which is thought to play a role in modulation of nociception in neuropathic states. Activation of galanin receptor 2 (GalR2) plays a pronociceptive role and enhances capsaicin-induced nociception in the periphery. GalR2 and vanilloid receptor 1 (VR1) are co-expressed in DRG neurons. Capsaicin evokes acute pain via activation of VR1 expressed in primary sensory neurons. It is not known to what extent galanin and its receptor GalR2 expression is regulated by capsaicin in DRG neurons. Effects of acute (4 h) or chronic (4 d) treatment with capsaicin at different concentrations (0.01, 0.1, 1 micromol/L) on galanin and GalR2 expression in primary cultured DRG neurons were investigated in the present study. Our results showed that acute exposure of high concentration capsaicin (1 micromol/L) increased galanin expression, whereas chronic exposure of low concentration capsaicin (0.01, 0.1 micromol/L) promoted galanin expression. Only chronic exposure of 0.1 micromol/L concentration capsaicin could elevate GalR2 expression, whereas capsaicin did not have this effect at any other conditions in this experiment. These results indicated that certain concentrations or exposure time of capsaicin stimulation may be relevant to upregulation of galanin and its receptor GalR2 expression in DRG cultures suggesting a response to peripheral neuronal stimulation. And also, capsaicin-induced GalR2 expression may be also modulated by capsaicin-induced galanin expression. The possible significance of the neurotransmission of nociceptive information involved in galanin or GalR2 expression caused by capsaicin is still to be clarified.
甘丙肽是一种由29个氨基酸组成的神经肽,在背根神经节(DRG)神经元中表达,被认为在神经病理性疼痛状态下的伤害感受调制中发挥作用。甘丙肽受体2(GalR2)的激活发挥促伤害感受作用,并增强辣椒素在外周引起的伤害感受。GalR2与香草酸受体1(VR1)在DRG神经元中共表达。辣椒素通过激活初级感觉神经元中表达的VR1引发急性疼痛。目前尚不清楚在DRG神经元中,甘丙肽及其受体GalR2的表达受辣椒素调控的程度。本研究调查了不同浓度(0.01、0.1、1微摩尔/升)的辣椒素急性(4小时)或慢性(4天)处理对原代培养的DRG神经元中甘丙肽和GalR2表达的影响。我们的结果表明,高浓度辣椒素(1微摩尔/升)急性暴露会增加甘丙肽表达,而低浓度辣椒素(0.01、0.1微摩尔/升)慢性暴露则促进甘丙肽表达。只有0.1微摩尔/升浓度的辣椒素慢性暴露能提高GalR2表达,而在本实验的任何其他条件下辣椒素均无此作用。这些结果表明,辣椒素刺激的特定浓度或暴露时间可能与DRG培养物中甘丙肽及其受体GalR2表达的上调有关,提示对周围神经元刺激的一种反应。此外,辣椒素诱导的GalR2表达可能也受辣椒素诱导的甘丙肽表达的调节。由辣椒素引起的甘丙肽或GalR2表达所涉及的伤害性信息神经传递的可能意义仍有待阐明。