Differential neuromodulation of calcium currents by norepinephrine in rat sympathetic neurons.
Differential neuromodulation of calcium currents by norepinephrine in rat sympathetic neurons.
复制标题
去甲肾上腺素对大鼠交感神经元钙电流的差异神经调节。
DOI：
10.1152/jn.1993.70.4.1440
复制
发表时间：
1993
影响因子：
2.5
通讯作者：
Schofield,GG
中科院分区：
文献类型：
--
作者：
Chen,C;Schofield,GG
1.用全细胞膜片钳技术研究了急性分离的大鼠颈上神经节(SCG)和更多的尾侧椎旁神经节(PVG)神经元对钙电流的神经调节差异。2.去甲肾上腺素(NE)对SCG和PVG神经元的钙电流均有浓度依赖性抑制作用。从浓度-反应曲线估算的去甲肾上腺素的半数抑制浓度(IC50)在SCG和PVG神经元中相似，但PVG神经元的最大抑制值低于SCG神经元。3.SCG和PVG神经元在去甲肾上腺素(5微米)或去甲肾上腺素(5微米)存在时的尾电流激活曲线均符合双Boltzmann方程。在NE存在的情况下，SCG和PVG神经元的激活曲线都向更多的去极化电位移动。SCG神经元的移位幅度大于PVG神经元，这可能是由于SCG神经元第一电流分量的分数幅度(增量1.4+/-0.4NA，均值+/-SE，39%)比PVG神经元(增量0.9+/-0.1NA，16%)下降更多(P<；0.05)。4.PVG神经元的钙电流密度大于SCG神经元，其最大尾电流幅度与细胞电容成正比。5.在SCG神经元，饱和浓度的Omega-CgTx(omega-CgTx)引起+20 mV时钙电流幅度的下降(77.4+/-1.9%)大于PVG神经元(71.2+/-1.5%，P<；0.05)。6.经15微米omega-CgTx处理后，NE对两种神经元的钙电流仍有抑制作用，但对SCG神经元的抑制作用(31.1+/-3.4%)大于PVG神经元(12.8+/-3.6%，P<；0.01)。7.二氢吡啶钙通道激动剂Bay K 8644(10微米)延长了SCG和PVG神经元的钙尾电流。归一化为细胞电容后，两组神经元对Bay K 8644诱发的尾电流幅值无显著差异。此外，NE(5微米)使由Bay K 8644(10微米)引起的延长的尾电流幅度在SCG增加44.7+/-13.5%，在PVG增加41.9+/11.9%。8.在对照条件下，去极化处理脉冲(50ms至+100 mV)可使PVG神经元(29.2+/-5.1%)和SCG神经元(20.1+/-4.0%)产生钙电流。
1. Differences in the neuromodulation of Ca2+ currents between superior cervical ganglion (SCG) and more caudal paravertebral ganglion (PVG) neurons acutely isolated from the same rats were investigated using the whole-cell patch-clamp technique. 2. Norepinephrine (NE) induced a concentration-dependent inhibition of Ca2+ currents in both SCG and PVG neurons. The concentration producing 50% inhibition (IC50) for NE estimated from concentration-response curves was similar between SCG and PVG neurons but the maximal inhibition estimated from the concentration-response curve for PVG neurons was decreased compared with that of SCG neurons. 3. Tail current activation curves of both SCG and PVG neurons in the absence and presence of NE (5 microM) could be fitted to a double Boltzmann equation. In the presence of NE, the activation curves for both SCG and PVG neurons were shifted toward more depolarized potentials. The magnitude of the shift was greater in SCG than in PVG neurons, which could be accounted for by a greater decrease (P < 0.05) in the fractional amplitude of the first current component of SCG neurons (delta 1.4 +/- 0.4 nA, mean +/- SE, 39%) compared with that of PVG neurons (delta 0.9 +/- 0.1 nA, 16%). 4. Ca2+ current density, expressed as maximal tail current amplitude normalized to cell capacitance, was greater in PVG neurons than that in SCG neurons. 5. In SCG neurons, a saturating concentration of omega-conotoxin GVIA (omega-CgTx) produced a greater decrease of Ca2+ current amplitude at +20 mV (77.4 +/- 1.9%) than in PVG neurons (71.2 +/- 1.5%, P < 0.05). 6. After pretreatment with 15 microM omega-CgTx, NE still decreased the Ca2+ currents in both populations of neurons; however, the inhibition was greater in SCG neurons (31.1 +/- 3.4%) than in PVG neurons (12.8 +/- 3.6%, P < 0.01). 7. The dihydropyridine Ca2+ channel "agonist" Bay K 8644 (10 microM) prolonged Ca2+ tail currents in both SCG and PVG neurons. After normalizing to cell capacitance, there was no significant difference in Bay K 8644-induced tail current amplitude between the two populations of neurons. Moreover, NE (5 microM) increased the prolonged Ca2+ tail current amplitude induced by Bay K 8644 (10 microM) by 44.7 +/- 13.5% in SCG and 41.9 +/- 11.9% in PVG neurons. 8. Under control conditions, Ca2+ currents were facilitated by a depolarizing conditioning pulse (50 ms to +100 mV) in both PVG neurons (29.2 +/- 5.1%) and SCG neurons (20.1 +/- 4.0%).(ABSTRACT TRUNCATED AT 400 WORDS)