乙酰胆碱对蟾蜍背根神经节神经元膜电位的影响及离子机制

在离体灌流的蟾蜍背根神经节(DRG)标本上,用微电极进行胞内记录。在73个神经元中,依神经纤维的传导速度将神经元分为 A 型及 C 型,其中 A 型细胞67个,C 型6个,静息膜电位为-67.5±1.3mV((?)±SE)。当加4×10~(-4)—6×10~(-4)mol/L 乙酰胆碱(ACh),可观察到如下四种膜电位变化:1.超极化:幅值9.1±3.0mV((?)±SE,n=23);(2)去极化:幅值12.9±2.2mV((?)+SE,n=20);(3)双相反应(n=24):先超极化,后去极化,超极化幅值8.0±2.4mV((?)+SE),去极化幅值10.9±3.1mV((?)±SE);(4)无反应(n=6)。用阿托品(1.3×10~(-5)mol/L,n=23),或同时应用筒箭毒与六甲双铵(浓度均为1.4×10~(-5)mol/L,n=8)灌流,能分别阻断 ACh 引起的膜的超极化或去极化。ACh 引起超极化反应时膜电导平均增加13.8%,翻转电位值大约-96mV。四乙铵(TEA,20mmol/L)能使 ACh 的去极化幅值增加48.2±3.2%((?)±SE,n=6),超极化幅值减小79.4±4.3%((?)±SE,n=8)。MnCl_2(4mmol/L)使 ACh 的去极化及超极化幅值分别减小54.2±7.2%((?)±SE,n=5)及69.2±6.4%((?)±SE,n=14)。以上结果提示:ACh 引起的 DRG 神经细胞膜去极化反应由 N 型乙酰胆碱受体介导,而超极化反应由 Μ 型乙酰胆碱受体介导,前者可能包含了多种离子电导的改变,后者则可能与钾电导增加有关。

EFFECT OF ACETYLCHOLINE ON MEMBRANE POTENTIAL IN TOAD DORSAL ROOT GANGLION NEURONS AND ITS IONIC BASIS

Intracellular recordings were made to investigate the effect of acetylcholine (ACh) on membrane potential of neurons in isolated toad dorsal root ganglion (DRG). In the 73 neurons examined, 67 were of type A, and the remaining 6 of type C cell. The resting membrane potential of these two types of cells was -67.5 +/- 1.3 mV (mean +/- SE). During the application of ACh (4 x 10(-4)-6 x 10(-4) mol/L) four types of the membrane potential changes were observed: (1) hyperpolarization of 9.1 +/- 3.0 mV (mean +/- SE, n = 23); (2) depolarization of 12.9 +/- 2.2 mV (mean +/- SE, n = 20); (3) biphasic response, i.e., hyperpolarization of 8.0 +/- 2.4 mV (mean +/- SE) followed by depolarization of 10.9 +/- 3.1 mV (mean +/- SE, n = 24); (4) no change (n = 6). The hyperpolarization induced by ACh could be blocked by atropine (1.3 x 10(-5) mol/L, n = 23), and ACh-induced depolarization could be abolished by coperfusion of d-tubocurarine (1.4 x 10(-5) mol/L) and hexamethonium (1.4 x 10(-5) mol/L, n = 18). During ACh hyperpolarization the membrane conductance was increased by 13.8% and the reversal potential was about -96 mV (n = 3). TEA (20 mmol/L) enhanced ACh depolarization amplitude by 48.2 +/- 3.2% (mean +/- SE, n = 6), and depressed ACh hyperpolarization by 79.4 +/- 4.3% (mean +/- SE, n = 8), MnCl2 (4 mmol/L) decreased the ACh depolarization and hyperpolarization by 54.2 +/- 7.2% (mean +/- SE, n = 5) and by 69.2 +/- 6.4% (mean +/- SE, n = 14) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)