Trudeau L E, Baux G, Fossier P, Tauc L
Laboratoire de Neurobiologie Cellulaire et Moléculaire, C.N.R.S., Gif-sur-Yvette, France.
Neuroscience. 1993 Mar;53(2):571-80. doi: 10.1016/0306-4522(93)90222-2.
The Ca2+ current recorded in the presynaptic neuron (B4/B5) of an identified Aplysia synapse was characterized in terms of its activation, voltage sensitivity, Ca2+ dependence of inactivation and pharmacology. It was compared to that recorded in left upper quadrant abdominal ganglion neurons which, unlike B4/B5, display Ca2+ action potentials. The two Ca2+ currents could not be distinguished in terms of their activation threshold or voltage sensitivity. The Ca2+ current recorded in left upper quadrant neurons, however, displayed more important Ca(2+)-dependent inactivation. The peak Ca2+ current in B4/B5 neurons was significantly reduced (30-40%) by the dihydropyridine Ca2+ channel antagonist, nifedipine, while it was increased (15-20%) by the dihydropyridine Ca2+ channel agonist, BAY K8644, although none of these agents had any effect on transmitter release from B4/B5. omega-Conotoxin similarly reduced the Ca2+ current by 30-40%, but unlike nifedipine, it also caused a 50-60% reduction in B4/B5 transmitter release. The pharmacological properties of the Ca2+ current present in left upper quadrant neurons were somewhat different, as this current was unaffected by either BAY K8644 or omega-conotoxin and moderately suppressed (20%) by nifedipine.
对已鉴定的海兔突触的突触前神经元（B4/B5）中记录的Ca2+电流，从其激活、电压敏感性、失活的Ca2+依赖性及药理学特性方面进行了表征。将其与左上腹神经节神经元中记录的Ca2+电流进行比较，与B4/B5不同，左上腹神经节神经元表现出Ca2+动作电位。这两种Ca2+电流在激活阈值或电压敏感性方面无法区分。然而，左上腹神经元中记录的Ca2+电流表现出更显著的Ca(2+)依赖性失活。二氢吡啶类Ca2+通道拮抗剂硝苯地平使B4/B5神经元中的Ca2+电流峰值显著降低（30 - 40%），而二氢吡啶类Ca2+通道激动剂BAY K8644使其增加（15 - 20%），尽管这些药物对B4/B5的递质释放均无影响。ω-芋螺毒素同样使Ca2+电流降低30 - 40%，但与硝苯地平不同的是，它还使B4/B5的递质释放减少50 - 60%。左上腹神经元中存在的Ca2+电流的药理学特性有所不同，因为该电流不受BAY K8644或ω-芋螺毒素的影响，而受硝苯地平适度抑制（20%）。
