Reciprocal synaptic interactions between rod bipolar cells and amacrine cells in the rat retina
Reciprocal synaptic interactions between rod bipolar cells and amacrine cells in the rat retina
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DOI：
10.1152/jn.1999.81.6.2923
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发表时间：
1999-06-01
影响因子：
2.5
通讯作者：
Hartveit, E
中科院分区：
文献类型：
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作者：
Hartveit, E
采用全细胞电压钳记录大鼠视网膜切片制备的杆状双极细胞，研究了杆状双极细胞与A17无突细胞之间的互交突触传递。杆状双极细胞的去极化引起了两种可识别的Ca2+电流，一种是激活在约-70 mV的t型电流，另一种是激活在约-50 mV的l型药理学电流。去极化至大于或等于-50 mV时，也会引起突触后电流（PSCs）频率的增加。这些PSCs的逆转与E-Cl（氯平衡电位）相似，跟随E-Cl的变化，并被γ -氨基丁酸（GABA）和GABA受体拮抗剂阻断，因此被鉴定为GABA能抑制性PSCs （IPSCs）。轴突切断的双极细胞显示t型电流，但缺乏l型电流和去极化诱导的ipsc。因此，l型Ca2+通道被战略性地放置在轴突末端，以介导杆状双极细胞的递质释放。非nmda受体拮抗剂6-cyano-7-nitroquinoxaline-2,3-dione阻断了IPSCs，表明非nmda受体介导了前馈双极到阿马分泌的兴奋。NMDA受体拮抗剂3-((RS)-2- carboxypperazin -4-yl)丙基-1-膦酸对去极化诱导的ipsc没有一致的作用，这表明NMDA受体的激活不是前馈激发所必需的。河豚毒素（一种电压门控Na+通道阻滞剂）在某些细胞中可逆地抑制了互反反应，但在其他细胞中却没有，这表明梯度电位足以使A17腺分泌细胞释放递质，但也表明电压门控Na+通道在某些条件下可以促进递质释放。
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 similar to E-Cl (the chloride equilibrium potential), followed changes in E-Cl, and were blocked by gamma-aminobutyric acid, (GABA,) and GABA, 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.