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与新生大鼠神经肌肉接头处神经递质释放相关的钙通道。

Calcium channels coupled to neurotransmitter release at neonatal rat neuromuscular junctions.

作者信息

Rosato Siri M D, Uchitel O D

机构信息

Laboratorio de Fisiología y Biología Molecular, Departamento de BiologíaFacultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Buenos Aires (1428), Argentina.

出版信息

J Physiol. 1999 Jan 15;514 ( Pt 2)(Pt 2):533-40. doi: 10.1111/j.1469-7793.1999.533ae.x.

Abstract
  1. The effects of different calcium channel blockers (omega-agatoxin IVA (omega-Aga IVA), omega-conotoxin GVIA (omega-CgTx GVIA) and dihydropyridines) were tested on spontaneous and evoked transmitter release at embryonic and newborn rat neuromuscular junctions (NMJs). 2. The nerve-evoked transmitter release quantal content (m) was strongly reduced by the P/Q-type voltage-dependent calcium channel (VDCC) blocker omega-Aga IVA (100 nM) at newly formed endplates of embryos and 0- to 11-day-old rats, in agreement with the effect of this blocker on transmitter release at mature and reinnervating muscles. 3. omega-CgTx GVIA (1-5 microM), the N-type VDCC blocker, also caused a significant reduction in m at newly formed NMJs early in development (embryos and 0- to 4-day-old rats), while it was ineffective in more mature animals (5- to 11-day-old rats). 4. L-type channel blockers, nitrendipine (1 microM) and nifedipine (1 microM), did not significantly affect neurally evoked release at developing NMJs. However, nifedipine (10 microM) was able to increase m significantly at 0- to 4-day-old rat NMJs. 5. At developing NMJs, K+-evoked transmitter release was dependent on Ca2+ entry through VDCCs of the P/Q-type family (100 nM omega-Aga IVA reduced 70 % of the K+-evoked miniature endplate potential frequency). N- and L-type VDCC blockers did not affect this type of release. 6. We conclude that at rat neuromuscular junctions the presynaptic calcium channel types involved in transmitter release undergo developmental changes during the early postnatal period.
摘要
  1. 测试了不同钙通道阻滞剂(ω-芋螺毒素IVA(ω-Aga IVA)、ω-芋螺毒素GVIA(ω-CgTx GVIA)和二氢吡啶类)对胚胎和新生大鼠神经肌肉接头(NMJ)处自发和诱发递质释放的影响。2. 在胚胎和0至11日龄大鼠新形成的终板处,P/Q型电压依赖性钙通道(VDCC)阻滞剂ω-Aga IVA(100 nM)可显著降低神经诱发的递质释放量子含量(m),这与该阻滞剂对成熟和再支配肌肉递质释放的作用一致。3. N型VDCC阻滞剂ω-CgTx GVIA(1 - 5 μM)在发育早期(胚胎和0至4日龄大鼠)新形成的NMJ处也导致m显著降低,而在更成熟的动物(5至11日龄大鼠)中则无效。4. L型通道阻滞剂尼群地平(1 μM)和硝苯地平(1 μM)对发育中的NMJ处神经诱发的释放没有显著影响。然而,硝苯地平(10 μM)能够显著增加0至4日龄大鼠NMJ处的m。5. 在发育中的NMJ处,K⁺诱发的递质释放依赖于通过P/Q型家族的VDCC进入的Ca²⁺(100 nM ω-Aga IVA使K⁺诱发的微小终板电位频率降低70%)。N型和L型VDCC阻滞剂不影响这种类型的释放。6. 我们得出结论,在大鼠神经肌肉接头处参与递质释放的突触前钙通道类型在出生后早期会发生发育变化。

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引用本文的文献

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1
Changes in end-plate activity produced by presynaptic polarization.突触前极化引起的终板活动变化。
J Physiol. 1954 Jun 28;124(3):586-604. doi: 10.1113/jphysiol.1954.sp005131.

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