Characterization of a P-type calcium current in a crayfish motoneuron and its selective modulation by impulse activity
Characterization of a P-type calcium current in a crayfish motoneuron and its selective modulation by impulse activity
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DOI：
10.1152/jn.1997.77.1.76
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发表时间：
1997-01-01
影响因子：
2.5
通讯作者：
Lnenicka, GA
中科院分区：
文献类型：
--
作者：
Hong, SJ;Lnenicka, GA
以往的研究表明，电压依赖性钙电流记录从细胞体的小龙虾腹部运动神经元，F3，经历了长期的减少，作为一个结果，增加冲动活动。使用双电极电压钳技术检查了经历这种长期变化的Ca 2+通道的特性。Ca 2+电流在-50至-40 mV时激活，其振幅在0 mV时最大（-135.0 +/- 25.8 nA，平均值+/- SE，n = 14）。Ca 2+通道对Cd ~（2+）的敏感性高于Ni ~（2+），表明Ca ~（2+）内流是通过高电压激活（HVA）的Ca ~（2+）通道进行的。散斑记录表明，Ca 2+电流产生的细胞体的膜。当Ba ~（2+）取代细胞外Ca ~（2+）时，内向电流的幅度增加40%，I-V关系负移约10 mV。应用P型钙通道拮抗剂欧米茄-agatoxin TVA（欧米茄-AgTX IVA）产生了一个显着的33%（n = 6）减少的Ba 2+电流的峰值幅度，而无论是L型钙通道拮抗剂硝苯地平或N型通道拮抗剂欧米茄-芋螺毒素GVIA产生的Ba 2+电流的减少。该P型（ω-AgTX-TVA敏感性）Ca 2+通道的电压依赖性激活与先前鉴定的P型通道相似，但不同于非P型（ω-AgTX-IVA抗性）Ca 2+通道。当在脉冲活动增加（5 Hz刺激45-60 min）后6-7 h测量Ca 2+电流时，P型电流的幅度降低了43%，但非P型电流的幅度没有显著变化。这些结果表明，至少有两种亚型的HVA Ca 2+通道有助于宏观Ca 2+电流中观察到的这种螯虾相运动神经元：一个属于先前描述的P型Ca 2+通道和其他（S）不属于N-，L-，或P-型Ca 2+通道。长期的，Ca 2+依赖性减少钙电流先前证明在运动神经元F3产生的选择性减少这种P型钙电流。这种活动依赖性减少的P-型钙电流可能参与长期抑郁症中观察到的神经肌肉突触的运动神经元的递质释放。
Previous studies have demonstrated that the voltage-dependent Ca2+ current recorded from the cell body of the crayfish abdominal motoneuron, F3, undergoes a long-term reduction as a result of increased impulse activity. The properties of the Ca2+ channels undergoing this long-term change were examined with the use of two-electrode voltage-clamp techniques. The Ca2+ current was activated at -50 to -40 mV and its amplitude was maximal at 0 mV (-135.0 +/- 25.8 nA, mean +/- SE, n = 14). The current-voltage relationship and the greater sensitivity of the Ca2+ channel to Cd2+ than Ni2+ indicated that Ca2+ influx occurs through high-voltage-activated (HVA) Ca2+ channels. Loose-patch recordings demonstrated that the Ca2+ current was generated by the membrane of the cell body. When Ba2+ was substituted for extracellular Ca2+ there was a 40% increase in the amplitude of the inward current and a negative shift of similar to 10 mV in the I-V relationship. Application of the P-type Ca2+ channel antagonist omega-agatoxin TVA (omega-AgTX IVA) produced a significant 33% (n = 6) reduction in the peak amplitude of the Ba2+ current, whereas neither the L-type Ca2+ channel antagonist nifedipine nor the N-type channel antagonist omega-conotoxin GVIA produced a reduction in the Ba2+ current. The voltage-dependent activation of this P-type (omega-AgTX-TVA-sensitive) Ca2+ channel was similar to previously identified P-type channels, but different from that of the non-P-type (omega-AgTX-IVA-resistant) Ca2+ channels. When Ca2+ currents were measured 6-7 h after an increase in impulse activity (5-Hz stimulation for 45-60 min), there was a 43% reduction in the amplitude of the P-type current, but no significant changes in the non-P-type current amplitude. These results demonstrate that at least two subtypes of HVA Ca2+ channels contribute to the macroscopic Ca2+ current observed in the cell body of this crayfish phasic motoneuron: one belongs to the previously described P-type Ca2+ channel and the other(s) does not belong to the N-, L-, or P-type Ca2+ channel. The long-term, Ca2+-dependent reduction in Ca2+ current previously demonstrated in motoneuron F3 is produced by the selective reduction of this P-type Ca2+ current. This activity-dependent reduction in the P-type Ca2+ current is likely involved in the long-term depression of transmitter release observed at the neuromuscular synapses of this motoneuron.