Hanse E, Gustafsson B
Department of Physiology, Göteborg University, Sweden.
Neuroscience. 1995 Aug;67(3):531-9. doi: 10.1016/0306-4522(95)00090-6.
The present study deals with the question of whether L-type voltage-gated calcium channels can support the induction of input specific long-term potentiation. Tetanus-induced potentiation of synaptic transmission was examined in the CA1 region of normal and disinhibited guinea-pig hippocampal slices. It was found that afferent tetanization in the presence of 50 microM of the N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid led to a prolonged input specific potentiation. This potentiation was found only in disinhibited slices, its induction required cooperativity, and it was associated with an increase in the early part of the field excitatory postsynaptic potential initial slope. It was not affected by the L-type voltage-gated calcium channel blocker nifedipine, but it was reduced when D(-)-2-amino-5-phosphonopentanoic acid was supplemented with other N-methyl-D-aspartate receptor antagonists. The present study also examined a potentiation that was not restricted to the activated synapses and that was not associated with an increase in the early part of the field excitatory postsynaptic potential initial slope. This potentiation was blocked by the L-type voltage-gated calcium channel antagonist nifedipine. It is concluded that calcium influx through L-type voltage-gated calcium channels participates in the generation of a prolonged potentiation, but not of the input specific N-methyl-D-aspartate receptor-dependent long-term potentiation. The results also suggest that high concentrations of D(-)-2-amino-5-phosphonopentanoic acid can be insufficient to fully prevent N-methyl-D-aspartate receptor activation by strong afferent tetanization in the disinhibited slice.
本研究探讨了L型电压门控钙通道是否能够支持输入特异性长时程增强的诱导。在正常和去抑制的豚鼠海马切片的CA1区检测了破伤风诱导的突触传递增强。结果发现，在存在50微摩尔N-甲基-D-天冬氨酸受体拮抗剂D-(-)-2-氨基-5-磷酸戊酸的情况下，传入强直刺激导致了一种持续时间延长的输入特异性增强。这种增强仅在去抑制的切片中发现，其诱导需要协同作用，并且与场兴奋性突触后电位初始斜率早期部分的增加有关。它不受L型电压门控钙通道阻滞剂硝苯地平的影响，但当D-(-)-2-氨基-5-磷酸戊酸与其他N-甲基-D-天冬氨酸受体拮抗剂合用时，这种增强会减弱。本研究还检测了一种不限于激活突触且与场兴奋性突触后电位初始斜率早期部分增加无关的增强。这种增强被L型电压门控钙通道拮抗剂硝苯地平阻断。得出的结论是，通过L型电压门控钙通道的钙内流参与了一种持续增强的产生，但不参与输入特异性N-甲基-D-天冬氨酸受体依赖性长时程增强的产生。结果还表明，高浓度的D-(-)-2-氨基-5-磷酸戊酸可能不足以完全阻止去抑制切片中强传入强直刺激对N-甲基-D-天冬氨酸受体的激活。
