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以培养的新生大鼠颈上交感节神经元为标本，使用膜片钳全细胞记录技术，观察了细胞外Ｃａ２＋对烟碱受体失敏的影响．发现向神经元喷射１００μｍｏｌ·Ｌ－１ＡＣｈ，可即刻诱发迅速上升的内向电流（ＡＣｈ电流）．随着胞外Ｃａ２＋浓度的上升，ＡＣｈ电流衰减明显加快（Ｐ＜０．０１）．而ＡＣｈ诱发电流的幅度和上升速率则随胞外Ｃａ２＋浓度的上升而显著增加（Ｐ＜０．０１）．当胞外Ｃａ２＋为０，２和６ｍｍｏｌ·Ｌ－１时，ＡＣｈ电流衰减的时间常数分别为８．０±４．３ｓ（ｎ＝９），４．２±０．９ｓ（ｎ＝８）和２．６±０．７ｓ（ｎ＝８）．诱发电流的幅度（ｎＡ）分别为２．０±０．９（ｎ＝９），３．３±１．０（ｎ＝８）和５．１±１．６（ｎ＝８）．其上升速率（ｐＡ／ｍｓ）分别为２．６±０．８和９．３±１．６（ｎ＝８）．以上结果说明，胞外Ｃａ２＋浓度的增加，可加速ＡＣｈ电流的衰减，即加速烟碱受体的失敏，同时提高ＡＣｈ电流幅度，加快烟碱受体离子孔道的开放速率．提示交感神经元烟碱受体上可能存在着不同的Ｃａ２＋结合位点．通过对这些不同位点的作用，Ｃａ２＋可以从两方面影响烟碱受体的功能，进而调制胆碱能神经元的突触传递效率．
The cultured neonatal rat sympathetic ganglion neurons were taken as a specimen and patch clamp whole cell recording technique was used to observe the effect of extracellular Ca2 + on nicotinic receptor desensitization. It was found that the injection of 100μmol·L-1ACh into the neurons induced a rapidly rising inward current (ACh current). With the increase of extracellular Ca2 + concentration, ACh current decay obviously accelerated (P <0.01). However, the amplitude and rate of ACh-induced current increased significantly with the increase of extracellular Ca2 + concentration (P <0.01). The ACh current decay time constants were 8.0 ± 4.3s (n = 9), 4.2 ± 0.9s (n = 8) and 2.6 ± 0.7 s (n = 8). The magnitude of induced current (nA) was 2.0 ± 0.9 (n = 9), 3.3 ± 1.0 (n = 8) and 5.1 ± 1.6 (n = 8), respectively. The rate of rise (pA / ms) was 2.6 ± 0.8 and 9.3 ± 1.6 (n = 8), respectively. The above results show that the increase of extracellular Ca2 + concentration can accelerate the decay of ACh current, which accelerates the desensitization of nicotinic acetylcholine receptor, increases the ACh current amplitude and accelerates the opening rate of nicotine receptor ion channel. Tip sympathetic neuronal nicotinic receptors may have different Ca2 + binding sites. By acting on these different sites, Ca2 + can affect nicotinic receptor function in two ways, thereby modulating the synaptic transmission efficiency of cholinergic neurons.