Capsaicin activation of glutamatergic synaptic transmission in the rat locus coeruleus in vitro

Capsaicin activation of glutamatergic synaptic transmission in the rat locus coeruleus in vitro
复制标题

DOI:
10.1113/jphysiol.2002.022863
复制
发表时间:
2002-09-01
影响因子:
5.5
通讯作者:
Connor, M
Connor, M
中科院分区:
医学1区
文献类型:
--
作者:
Marinelli, S;Vaughan, CW;Connor, M

文献摘要

被引文献

相似文献

香草酸受体蛋白(VR 1)是一个很好的特点,在外周感觉神经元的伤害性刺激的集成商。有证据表明VR 1存在于中枢神经系统中,但关于其作用的信息很少。在这项研究中,我们研究了VR 1受体激动剂在大鼠蓝斑(LC)的行动,使用全细胞膜片钳记录急性分离的神经元和神经元切片。辣椒素灌流导致LC神经元孤立的微型兴奋性突触后电流(mEPSC)的频率呈浓度依赖性增加。辣椒素对mEPSCs的平均振幅没有影响。辣椒素(1 μ m)的影响被VR 1受体拮抗剂辣椒平(10 μ m)和碘树脂毒素(300 nm)消除。去除细胞外Ca 2+消除辣椒素诱导的mEPSCs频率的增加。辣椒素灌流对诱发的兴奋性突触后电流没有一致的影响。辣椒素灌流也导致肾上腺素能受体激动剂在LC中的释放,但不影响急性分离的LC神经元的膜电流。这些数据表明,VR 1受体似乎位于突触前的传入LC,VR 1的激活可能有助于加强释放谷氨酸和肾上腺素/去甲肾上腺素在这个脑区。
The vanilloid receptor protein (VR1) is a well-characterised integrator of noxious stimuli in peripheral sensory neurones. There is evidence for the presence of VR1 in the central nervous system, but little information as to its role there. In this study we have examined the actions of agonists for VR1 receptors in the rat locus coeruleus (LC), using whole-cell patch-clamp recordings from acutely isolated neurones and neurones in slices. Superfusion with capsaicin resulted in a concentration-dependent increase in the frequency of isolated miniature excitatory postsynaptic currents (mEPSCs) in LC neurones. The mean amplitude of the mEPSCs was not affected by capsaicin. The effects of capsaicin (1 mum) were abolished by the VR1 receptor antagonists capsazepine (10 mum) and iodoresiniferatoxin (300 nm). Removal of extracellular Ca2+ abolished the capsaicin-induced increase in frequency of mEPSCs. Capsaicin superfusion had no consistent effects on evoked excitatory postsynaptic currents. Capsaicin superfusion also resulted in the release of an adrenoceptor agonist in the LC but did not affect the membrane currents of acutely isolated LC neurones. These data demonstrate that the VR1 receptor appears to be located presynaptically on afferents to the LC, and that activation of VR1 may serve to potentiate the release of glutamate and adrenaline/noradrenaline in this brain region.