The actions of anandamide on rat superficial medullary dorsal horn neurons in vitro
The actions of anandamide on rat superficial medullary dorsal horn neurons in vitro
复制标题
阿那达酰胺对体外大鼠浅髓背角神经元的作用
DOI：
10.1111/j.1469-7793.2003.00121.x
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
M. Christie
中科院分区：
文献类型：
--
作者：
E. Jennings;C. Vaughan;C. Vaughan;L. A. Roberts;M. Christie
体外对三叉神经尾核和三叉神经节神经元进行全细胞膜片钳记录，研究内源性大麻素anandamide的细胞作用。Anandamide已被证明通过大麻素受体1 （CB1）和香草素受体1 （VR1）起作用。Anandamide （30 μm）导致微型兴奋性突触后电流（mepsc）的速率增加54%，而不影响其振幅。anandamide的作用被VR1拮抗剂capsazepine （20 μm）阻断，但不被CB1特异性拮抗剂AM251 （3 μm）阻断。应用VR1受体激动剂辣椒素（300 nm）可使mEPSC率提高4200%。在解离的三叉神经节神经元中，anandamide和辣椒素都在+40 mV电压箝位的神经元中引起外向电流。辣椒胺（EC50, 10 μm）产生的最大外向电流为辣椒素（10 μm）的45%。VR1拮抗剂capsazepine （30 μm）的共同应用完全逆转了辣椒素和anandamide的作用。anandamide转运抑制剂AM404 （30 μm）使mEPSC率增加40%，并在游离神经元中产生外向电流。后一种电流被VR1拮抗剂碘胺干扰素（1 μm）逆转。脂肪酸酰胺水解酶（FAAH）抑制剂苯基甲基磺酰氟（PMSF） （20 μm）和OL53 （1 μm）在薄片或游离神经元制备中均没有增强anandamide的作用。这些结果表明，在浅髓背角内，anandamide （30 μm）通过激活VR1受体，在突触前增强谷氨酸的释放。
Whole‐cell patch‐clamp recordings were made from neurons in the trigeminal nucleus caudalis and trigeminal ganglion, in vitro, to investigate the cellular actions of the endogenous cannabinoid, anandamide. Anandamide has been shown to act through both the cannabinoid receptor 1 (CB1) and the vanilloid receptor 1 (VR1). Anandamide (30 μm) caused a 54 % increase in the rate of miniature excitatory post‐synaptic currents (mEPSCs), without affecting their amplitude. The effect of anandamide was blocked by the VR1 antagonist capsazepine (20 μm), but not by the CB1‐specific antagonist AM251 (3 μm). Application of the VR1 receptor agonist capsaicin (300 nm) caused a 4200 % increase in the mEPSC rate. In dissociated trigeminal ganglion neurons, both anandamide and capsaicin caused an outward current in neurons that were voltage clamped at +40 mV. The maximal outward current produced by anandamide (EC50, 10 μm) was 45 % of that produced by capsaicin (10 μm). Co‐application of the VR1 antagonist capsazepine (30 μm) completely reversed the effects of both capsaicin and anandamide. The anandamide transport inhibitor, AM404 (30 μm) caused a 40 % increase in mEPSC rate in the slice preparation and an outward current in dissociated neurons. The latter current was reversed by the VR1 antagonist iodoresiniferatoxin (1 μm). The fatty acid amide hydrolase (FAAH) inhibitors phenylmethylsulfonyl fluoride (PMSF) (20 μm) and OL53 (1 μm) did not enhance the effect of anandamide in either the slice or dissociated neuron preparations. These results suggest that within the superficial medullary dorsal horn, anandamide (30 μm) acts presynaptically to enhance the release of glutamate via activation of the VR1 receptor.
DOI：
10.1073/pnas.96.21.12198
发表时间：
1999-10-12
影响因子：
11.1
作者：
Walker, JM;Huang, SM;Sañudo-Peña, MC
通讯作者：
Sañudo-Peña, MC
影响因子：
56.9
作者：
DEVANE, WA;HANUS, L;MECHOULAM, R
通讯作者：
MECHOULAM, R
DOI：
10.1073/pnas.97.10.5044
发表时间：
2000-05-09
影响因子：
11.1
作者：
Boger, DL;Sato, H;Cravatt, BF
通讯作者：
Cravatt, BF