THE TEMPERATURE-DEPENDENCE OF HIGH-THRESHOLD CALCIUM-CHANNEL CURRENTS RECORDED FROM ADULT-RAT DORSAL RAPHE NEURONS
THE TEMPERATURE-DEPENDENCE OF HIGH-THRESHOLD CALCIUM-CHANNEL CURRENTS RECORDED FROM ADULT-RAT DORSAL RAPHE NEURONS
复制标题
DOI：
10.1016/0028-3908(95)00130-x
复制
发表时间：
1995-11-01
影响因子：
4.7
通讯作者：
KELLY, JS
中科院分区：
文献类型：
--
作者：
MCALLISTERWILLIAMS, RH;KELLY, JS
在急性分离的成年大鼠中缝背侧神经元上，以Ba2+为电荷载体，研究了HVA钙通道电流的温度依赖性。电流幅值具有很高的灵敏度，Q(10)介于1.7和2.5之间。电流中最敏感的成分是从超极化保持电位中激活的电流，并在200毫秒的测试脉冲中失活。最不敏感的是由去极化电位产生的更持久的电流。温度的升高也会导致电流-电压关系在超极化方向上发生不可逆的移动。到目前为止，对温度最敏感的性质是活化时间常数，其异常Q(10)介于10和12之间。这不受保持电位的显著影响，尽管时间常数本身取决于测试电位。温度升高到25摄氏度或更高时，显示出一种快速失活的成分，在较低温度下看不到。这些结果表明，在中缝背侧神经元中至少存在三种HVA电流成分。此外，激活动力学的高Q(10)表明，钙通道电流激活的过程是多方面的和复杂的。本文提出了一种新的假说，试图解释神经递质调节HVA钙通道电流激活动力学的方式。
The temperature dependence of HVA calcium channel currents, using barium as the charge carrier, was studied in acutely isolated adult rat dorsal raphe neurones. Current amplitude was found to be highly sensitive with a Q(10) of between 1.7 and 2.5. The most sensitive component of current is that that is activated from hyperpolarized holding potentials, and inactivates during a 200 msec test pulse. The least sensitive is the more sustained current elicited from depolarized potentials. Increases in temperature were also found to cause an irreversible shift in the current-voltage relationship in the hyperpolarizing direction. By far the most temperature-sensitive property was the activation time constant with an extraordinary Q(10) of between 10 and 12. This was not significantly affected by holding potential, though the time constant itself is dependent on the test potential. Increases in temperature to 25 degrees C or above revealed a fast inactivating component, not seen at lower temperatures. These findings suggest that there are at least three components of HVA current in dorsal raphe neurones. In addition, the remarkably high Q(10) for activation kinetics suggests that the processes underlying calcium channel current activation are multifaceted and complex. The following paper puts forward a new hypothesis which attempts to explain the way in which neurotransmitters modulate the activation kinetics of HVA calcium channel currents.