Yoshimura M, Polosa C, Nishi S
J Neurophysiol. 1987 May;57(5):1314-24. doi: 10.1152/jn.1987.57.5.1314.
Sympathetic preganglionic neurons of the intermediolateral nucleus were identified by antidromic stimulation in the slice of the T2 or T3 segment of the cat spinal cord. In normal Krebs solution, the action potential of these neurons had a shoulder on the repolarization phase and was followed by a long-lasting afterhyperpolarization (AHP). The AHP had a fast and a slow component. Superfusion of the slice with noradrenaline (NA), 10-50 microM, resulted in depression of the shoulder on the repolarization phase of the action potential, in the appearance of an afterdepolarization (ADP), which was absent in control conditions, and in depression of the slow component of the AHP. These effects were present whether the membrane potential of the sympathetic preganglionic neurons was decreased, increased, or not changed by NA. A typical ADP had time to peak of 50 ms and decay time of 200-500 ms; the amplitude was variable and large ADPs could be suprathreshold, causing repetitive firing. The amplitude and duration of the ADP increased with NA concentration. The appearance of the ADP seemed to be independent of the depressant effect of NA on the slow AHP. The ADP was associated with a decrease in neuron input resistance and was voltage dependent, being depressed in nonlinear fashion by membrane hyperpolarization. The ADP decreased in amplitude or disappeared within a range of membrane potentials from -70 to -90 mV. The ADP was reversibly suppressed by the Ca-channel blocker cobalt (2 mM), by low Ca Krebs (0.25 mM), and by iontophoretic injection of ethyleneglycol-bis(B-aminoethyl-ether)-N,N'-tetraacetic acid into the cell. Increasing Ca concentration from 2.5 to 10.0 mM had no effect. The ADP was unaffected by tetrodotoxin, at a concentration blocking the Na spike, but was suppressed in Na-free medium, even when the Ca spike was prolonged by tetraethylammonium 20 mM. Changes in external K concentration from 3.6 to 2.5 or 10.0 mM did not change the ADP. Increasing intracellular Cl concentration or decreasing extracellular Cl concentration had no effect on the ADP. It is concluded that the ADP, evoked by NA, is due to an increase in membrane conductance involving Na and Ca ions, possibly a Ca-activated Na conductance. The ADP provides a mechanism with which NA may modulate sympathetic preganglionic neuron responsiveness to excitatory synaptic inputs.
通过对猫脊髓T2或T3节段切片进行逆向刺激，鉴定出中间外侧核的交感神经节前神经元。在正常的Krebs溶液中，这些神经元的动作电位在复极化阶段有一个肩峰，随后是一个持久的超极化后电位（AHP）。AHP有一个快速成分和一个慢速成分。用10 - 50微摩尔的去甲肾上腺素（NA）对切片进行灌流，导致动作电位复极化阶段的肩峰降低，出现了对照条件下不存在的去极化后电位（ADP），并且AHP的慢速成分降低。无论交感神经节前神经元的膜电位是因NA而降低、升高还是未改变，这些效应都存在。典型的ADP达到峰值的时间为50毫秒，衰减时间为200 - 500毫秒；其幅度可变，大的ADP可能超过阈值，导致重复放电。ADP的幅度和持续时间随NA浓度增加。ADP的出现似乎与NA对慢速AHP的抑制作用无关。ADP与神经元输入电阻的降低有关，并且是电压依赖性的，通过膜超极化以非线性方式受到抑制。在膜电位从 - 70到 - 90毫伏的范围内，ADP的幅度降低或消失。ADP可被钙通道阻滞剂钴（2毫摩尔）、低钙Krebs溶液（0.25毫摩尔）以及通过向细胞内离子电泳注射乙二醇 - 双（β - 氨基乙基醚） - N，N' - 四乙酸可逆地抑制。将钙浓度从2.5毫摩尔增加到10.0毫摩尔没有影响。ADP不受能阻断钠峰的河豚毒素浓度的影响，但在无钠培养基中受到抑制，即使当钙峰被20毫摩尔的四乙铵延长时也是如此。细胞外钾浓度从3.6毫摩尔变为2.5毫摩尔或10.0毫摩尔不会改变ADP。增加细胞内氯浓度或降低细胞外氯浓度对ADP没有影响。得出的结论是，由NA诱发的ADP是由于涉及钠和钙的膜电导增加，可能是一种钙激活的钠电导。ADP提供了一种机制，通过该机制NA可以调节交感神经节前神经元对兴奋性突触输入的反应性。
