Caeser M, Brown D A, Gähwiler B H, Knöpfel T
Brain Research Institute, University of Zürich, Switzerland.
Eur J Neurosci. 1993 Jun 1;5(6):560-9. doi: 10.1111/j.1460-9568.1993.tb00521.x.
A depolarization-induced, slowly decaying inward current was examined in slice-cultured CA3 pyramidal cells by voltage-clamp techniques and microfluorometric measurements of cytosolic free Ca2+ concentration ([Ca2+]i). Action potentials elicited by intracellular injection of short-lasting (50-100 ms) depolarizing current pulses were followed by a slowly decaying afterhyperpolarization (AHP). After switching to voltage-clamp mode, short-lasting (50-100 ms) depolarizing voltage jumps from -60 mV to between -30 and 0 mV induced a slowly decaying outward aftercurrent (IAHP) which was depressed by bath application of muscarine (0.5 microM). In the presence of muscarine, the same depolarizations induced a slowly decaying afterdepolarization (ADP) or inward aftercurrent (IADP) in voltage-clamp mode. This current was also induced in the presence of trans(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (t-ACPD, 5 microM), an agonist of metabotropic glutamate receptors, but not in the presence of noradrenalin (5 microM), while both of these agonists depressed IAHP. IADP was depressed by reducing the external Ca2+ concentration from 3.8 to 0.5 mM, by external Co2+ (1 mM) and by external Cd2+ (10-100 microM). Combined voltage-clamp recordings and microfluorometric measurements of [Ca2+]i using the Ca2+ indicator fura-2 revealed that the amplitude of IADP was correlated with the amplitude of depolarization-induced Ca2+ influx. IADP was absent at membrane potentials < -90 mV, and reached maximal amplitudes at approximately -55 mV. Raising the extracellular K+ concentration from 2.7 to 13.5 mM increased the amplitude of IADP and resulted in a positively directed shift of the apparent reversal potential of IADP. When the external Na+ concentration was reduced from 157 to 33 or 18 mM the current reversed at more negative potentials and was reduced to 40 and 21%, respectively, of control amplitude. Lowering the external CI- concentration from 159 to 20 mM did not affect IADP. We conclude that IADP most likely represents a Ca(2+)-activated cation current, rather than a Ca2+ tail current, or an electrogenic Ca2+ extrusion current.
采用电压钳技术和细胞溶质游离钙离子浓度([Ca2+]i)的显微荧光测定法,在切片培养的CA3锥体神经元中检测了一种去极化诱导的、缓慢衰减的内向电流。通过细胞内注入短持续时间(50 - 100毫秒)的去极化电流脉冲引发动作电位后,会跟随一个缓慢衰减的超极化后电位(AHP)。切换到电压钳模式后,从 -60 mV到 -30至0 mV的短持续时间(50 - 100毫秒)去极化电压阶跃会诱导出一个缓慢衰减的外向尾电流(IAHP),该电流会被浴槽施加毒蕈碱(0.5微摩尔)所抑制。在毒蕈碱存在的情况下,相同的去极化在电压钳模式下会诱导出一个缓慢衰减的去极化后电位(ADP)或内向尾电流(IADP)。这种电流在代谢型谷氨酸受体激动剂反式(±)-1-氨基-1,3-环戊烷二羧酸(t-ACPD,5微摩尔)存在时也会被诱导产生,但在去甲肾上腺素(5微摩尔)存在时则不会,而这两种激动剂都会抑制IAHP。通过将细胞外Ca2+浓度从3.8 mM降低到0.5 mM、加入细胞外Co2+(1 mM)和细胞外Cd2+(10 - 100微摩尔),IADP会受到抑制。使用钙离子指示剂fura-2进行的联合电压钳记录和[Ca2+]i的显微荧光测定显示,IADP的幅度与去极化诱导的Ca2+内流幅度相关。IADP在膜电位 < -90 mV时不存在,在约 -55 mV时达到最大幅度。将细胞外K+浓度从2.7 mM提高到13.5 mM会增加IADP的幅度,并导致IADP的表观反转电位正向偏移。当细胞外Na+浓度从157 mM降低到33 mM或18 mM时,电流在更负的电位处反转,并且分别降低到对照幅度的40%和21%。将细胞外Cl-浓度从159 mM降低到20 mM不会影响IADP。我们得出结论,IADP很可能代表一种Ca(2+)-激活的阳离子电流,而不是Ca2+尾电流或生电Ca2+外流电流。