Segal M
Brain Res. 1981 Feb 9;206(1):107-28. doi: 10.1016/0006-8993(81)90104-9.
The ionic basis of norepinephrine (NE) action was studied with intracellular recording techniques in the rat hippocampal slice. Topical application of NE caused, in CA1 neurons, a 3-4 mV hyperpolarization associated with a 10-20% decrease in input resistance. This effect was accompanied by a decrease in spontaneous action potential discharges and, in some cells, by a reduction in EPSPs produced by stimulation of the excitatory Schaffer collateral-commissural pathway. An analysis of the voltage and concentration dependency revealed that NE may activate two different mechanisms. Experiments performed to test this hypothesis have demonstrated that a short duration hyperpolarizing action of NE was still present in a low Cl- medium. The hyperpolarizing responses to NE were absent in ouabain-treated slices and in low temperature. Cyclic AMP produced a 3-4 mV hyperpolarization associated with minimal changes in input resistance. This effect of cAMP was blocked by ouabain. IBMX potentiated responses to low concentrations of NE. It is proposed that NE activates two mechanisms; one involves activation of Cl- conductance and the other activation of a Na+-K+ pump. This latter effect might be mediated by cAMP.
采用细胞内记录技术在大鼠海马切片中研究了去甲肾上腺素（NE）作用的离子基础。在CA1神经元中，局部应用NE可引起3 - 4 mV的超极化，同时输入电阻降低10 - 20%。这种效应伴随着自发放电动作电位的减少，在一些细胞中，还伴随着刺激兴奋性的谢弗侧支-连合通路所产生的兴奋性突触后电位（EPSP）的降低。对电压和浓度依赖性的分析表明，NE可能激活两种不同的机制。为验证这一假设所进行的实验表明，在低Cl-培养基中，NE的短时间超极化作用仍然存在。在哇巴因处理的切片和低温条件下，对NE的超极化反应消失。环磷酸腺苷（cAMP）可产生3 - 4 mV的超极化，同时输入电阻变化最小。cAMP的这种效应被哇巴因阻断。异丁基甲基黄嘌呤（IBMX）增强了对低浓度NE的反应。有人提出，NE激活两种机制；一种涉及Cl-电导的激活，另一种涉及Na+-K+泵的激活。后一种效应可能由cAMP介导。
