Hartveit E
Department of Anatomy and Cell Biology, University of Bergen, N-5009 Bergen, Norway.
J Neurophysiol. 1999 Jun;81(6):2923-36. doi: 10.1152/jn.1999.81.6.2923.
Reciprocal synaptic transmission between rod bipolar cells and presumed A17 amacrine cells was studied by whole cell voltage-clamp recording of rod bipolar cells in a rat retinal slice preparation. Depolarization of a rod bipolar cell evoked two identifiable types of Ca2+ current, a T-type current that activated at about -70 mV and a current with L-type pharmacology that activated at about -50 mV. Depolarization to greater than or equal to -50 mV also evoked an increase in the frequency of postsynaptic currents (PSCs). The PSCs reversed at approximately ECl (the chloride equilibrium potential), followed changes in ECl, and were blocked by gamma-aminobutyric acidA (GABAA) and GABAC receptor antagonists and thus were identified as GABAergic inhibitory PSCs (IPSCs). Bipolar cells with cut axons displayed the T-type current but lacked an L-type current and depolarization-evoked IPSCs. Thus L-type Ca2+ channels are placed strategically at the axon terminals to mediate transmitter release from rod bipolar cells. The IPSCs were blocked by the non-N-methyl-D-aspartate (non-NMDA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, indicating that non-NMDA receptors mediate the feed-forward bipolar-to-amacrine excitation. The NMDA receptor antagonist 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid had no consistent effect on the depolarization-evoked IPSCs, indicating that activation of NMDA receptors is not essential for the feedforward excitation. Tetrodotoxin (a blocker of voltage-gated Na+ channels) reversibly suppressed the reciprocal response in some cells but not in others, indicating that graded potentials are sufficient for transmitter release from A17 amacrine cells, but suggesting that voltage-gated Na+ channels, under some conditions, can contribute to transmitter release.
通过对大鼠视网膜切片标本中的视杆双极细胞进行全细胞电压钳记录，研究了视杆双极细胞与假定的A17无长突细胞之间的相互突触传递。对视杆双极细胞进行去极化可诱发两种可识别的Ca2+电流类型，一种是在约-70 mV时激活的T型电流，另一种是具有L型药理学特性、在约-50 mV时激活的电流。去极化至大于或等于-50 mV也会引起突触后电流（PSC）频率增加。PSC在约ECl（氯离子平衡电位）处反转，随ECl变化，且被γ-氨基丁酸A（GABAA）和GABAC受体拮抗剂阻断，因此被鉴定为GABA能抑制性PSC（IPSC）。轴突被切断的双极细胞表现出T型电流，但缺乏L型电流和去极化诱发的IPSC。因此，L型Ca2+通道战略性地位于轴突末端，以介导视杆双极细胞释放递质。IPSC被非N-甲基-D-天冬氨酸（非NMDA）受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮阻断，表明非NMDA受体介导前馈性双极细胞到无长突细胞的兴奋。NMDA受体拮抗剂3-((RS)-2-羧基哌嗪-4-基)-丙基-1-膦酸对去极化诱发的IPSC没有一致的影响，表明NMDA受体的激活对于前馈性兴奋并非必不可少。河豚毒素（一种电压门控Na+通道阻滞剂）在一些细胞中可逆地抑制相互反应，但在其他细胞中则不然，这表明分级电位足以使A17无长突细胞释放递质，但也表明在某些条件下，电压门控Na+通道可能有助于递质释放。
