Characterization of inhibitory postsynaptic currents in rod bipolar cells of the mouse retina

被引:24
作者
Frech, MJ
Backus, KH
机构
[1] Goethe Univ Frankfurt, Inst Physiol 2, D-60590 Frankfurt, Germany
[2] Max Planck Inst Hirnforsch, Neuroanat Dept, D-60528 Frankfurt, Germany
关键词
patch-clamp; postsynaptic currents; GABAA receptor; GABA(C) receptor; glycine receptor;
D O I
10.1017/S0952523804214134
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The synaptic terminals of mammalian rod bipolar cells are the targets of multiple presynaptic inhibitory inputs arriving from glycinergic and GABAergic amacrine cells. To investigate the contribution of these different inhibitory receptor types, we have applied the patch-clamp technique in acutely isolated slices of the adult mouse retina. By using the whole-cell configuration, we measured and analyzed the spontaneous postsynaptic currents (PSCs) in rod bipolar cells. The spontaneous synaptic activity of rod bipolar cells was very low. However, when amacrine cells were depolarized by AMPA or kainate, the PSC frequency in rod bipolar cells increased significantly. These PSCs comprised several types that could be distinguished by pharmacological and kinetic criteria. Strychnine-sensitive, glycinergic PSCs were characterized by a mean peak amplitude of -43.5 pA and a weighted decay time constant (tau(w)) of 10.9 ms. PSCs that persisted in the presence of strychnine, but were completely inhibited by bicuculline, were mediated by GABA(A)Rs. They had a mean peak amplitude of -20.0 pA and a significantly faster tauw of 5.8 ms. Few PSCs remained in the presence of strychnine and bicuculline, suggesting that they were mediated by GABA(C)Rs. These PSCs were characterized by much smaller amplitudes (-6.2 pA) and a significantly slower decay kinetics (tau(w) = 51.0 ms). We conclude that rod bipolar cells express at least three types of functionally different inhibitory receptors, namely GABA(A)Rs, GABA(C)Rs, and GlyRs that may ultimately regulate the Ca2+ influx into rod bipolar cell terminals, thereby modulating their glutamate release.
引用
收藏
页码:645 / 652
页数:8
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