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Calcium conductance and firing properties of spinal motoneurones in the turtle.

机译:钙电导率和射击性质的脊椎运动神经元。

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摘要

1. The contribution of Ca2+ conductance to the firing properties of motoneurones was investigated in transverse slices of the turtle spinal cord. 2. In the presence of tetrodotoxin (TTX), tetraethylamonium (TEA) in low extracellular concentration (less than 5 mM) promoted Ca2+ spikes. In higher concentrations of TEA, a suprathreshold depolarizing current pulse was followed by an after-discharge of Ca2+ spikes riding on a Ca2+ plateau potential. 3. The Ca2+-dependent plateau was also promoted by Cs+, 4-aminopyridine (4-AP) and apamin. However, Ca2+ spikes during plateaux were an order of magnitude faster when promoted by Cs+ or 4-AP rather than TEA, and apamin did not promote Ca2+ spikes at all. 4. Ca2+ plateaux but not Ca2+ spikes were blocked by nifedipine. 5. In normal medium all effects of the transient Ca2+ influx during action potentials were attributable to its influence on the slow after-hyperpolarization. The nifedipine-sensitive, sustained Ca2+ influx was expressed exclusively as plateau potentials and only under conditions of reduced K+ current. 6. It is concluded that the transient and the sustained Ca2+ fluxes in spinal motoneurones are curtailed by different K+ conductances. The two Ca2+ responses are suggested as being mediated by two different types of Ca2+ channels.
机译:1.在龟脊髓横切片中研究了Ca2 +电导对运动神经元放电特性的影响。 2.在存在河豚毒素(TTX)的情况下,低细胞外浓度(小于5 mM)的四乙铵(TEA)会促进Ca2 +峰值。在较高浓度的TEA中,超阈值去极化电流脉冲之后是Ca2 +平台电位上的Ca2 +尖峰的后放电。 3. Cs +,4-氨基吡啶(4-AP)和Apapamin也促进了Ca2 +依赖性平台期。然而,当由Cs +或4-AP而不是TEA促进时,高原期的Ca2 +峰值快一个数量级,而apamin根本不促进Ca2 +峰值。 4.硝苯地平阻滞了Ca2 +平台性而非Ca2 +峰值。 5.在正常介质中,动作电位期间瞬时Ca2 +流入的所有影响均归因于其对缓慢的超极化后的影响。硝苯地平敏感的,持续的Ca2 +内流仅以高原电位表示,并且仅在K +电流降低的条件下表达。 6.结论是,脊髓运动神经元中瞬时的Ca2 +通量和持续的Ca2 +通量受到不同的K +电导率的限制。提示这两种Ca2 +响应是由两种不同类型的Ca2 +通道介导的。

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