Blanton K J, Kriegstein A R
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.
Brain Res. 1992 Jan 20;570(1-2):42-8. doi: 10.1016/0006-8993(92)90561-m.
Whole-cell voltage and current clamp recordings were obtained from cortical neurons of the pond turtle, Pseudemys scripta elegans. Norepinephrine (NE) induced an outward current in 50% of pyramidal neurons. This current had a reversal potential of -88.3 +/- 3.2 mV, consistent with a K+ conductance increase, and had a mean amplitude of 18.3 +/- 7.2 pA at -40 mV. The ionic dependence and pharmacological analyses are both consistent with alpha 2 adrenergic receptor stimulation. Inhibition of Na(+)-dependent action potentials with TTX did not diminish the NE-induced K+ conductance, indicating that NE acts directly on the postsynaptic neuron. In addition to effects on postsynaptic conductance, NE dramatically decreased the amplitude of spontaneous inhibitory postsynaptic currents (IPSCs) in 55% of pyramidal neurons. The decrease in spontaneous IPSCs was observed both in those neurons which exhibited an increase in K+ conductance in response to NE administration (81%) and in those which did not (33%). Thus, NE modulates neuronal excitability both directly by activating a postsynaptic K+ conductance and indirectly by decreasing spontaneous IPSCs.
全细胞电压钳和电流钳记录是从秀丽锦龟的皮质神经元获得的。去甲肾上腺素(NE)在50%的锥体神经元中诱导出外向电流。该电流的反转电位为-88.3±3.2 mV,与钾离子电导增加一致,在-40 mV时平均幅度为18.3±7.2 pA。离子依赖性和药理学分析均与α2肾上腺素能受体刺激一致。用河豚毒素(TTX)抑制钠依赖性动作电位并没有减弱NE诱导的钾离子电导,这表明NE直接作用于突触后神经元。除了对突触后电导的影响外,NE还使55%的锥体神经元中自发抑制性突触后电流(IPSC)的幅度显著降低。在那些对NE给药有钾离子电导增加反应的神经元(81%)和没有这种反应的神经元(33%)中均观察到自发IPSC的减少。因此,NE通过激活突触后钾离子电导直接调节神经元兴奋性,并通过减少自发IPSC间接调节神经元兴奋性。