| Input Receptors |
| Axon terminal |
| ; amacrine | Gaba |
| GABA(A) and GABA(C) receptor-mediated currents were observed in the isolated terminal (Pan ZH, 2001374 ).
Isolated rod-dominant on-center bipolar cells respond to GABA, the highest sensitivity of which being located at the axon terminal (Tachibana M and Kaneko A, 1987386 ). Zn2+ modulates the inhibitory interaction between amacrine and bipolar cells, particularly that mediated by the GABA(C) receptor(Kaneda and Andrasfalvy B and Kaneko A, 2000387 ) In retinal bipolar cells of bullfrog, both axon terminals and dendrites showed high GABA sensitivity mediated by both GABA(A) and GABA(C) receptors. GABA(A) and GABA(C) receptors may play different roles in the outer and inner retina and the differential complements of the two receptors on OFF and ON BCs may be closely related to physiological functions of these cells (Du JL and Yang XL, 2000395 ). GABA(A) receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell (Shields CR, Tran M and Wong RO and Lukasiewicz PD, 2000396 ).
; The rod-dominant ON-type bipolar cells and some bipolar cells with a small axon terminal receive negative feedback inputs from GABAergic amacrine cells (Tachibana M and Kaneko A, 1988384 ). Depolarization induced transient outward currents that resembled IPSCs and were blocked by GABA and glycine receptor antagonists, suggesting that they arise from activation of amacrine feedback synapses (Protti DA and Llano I, 1998378 ). The OFF cone bipolar cells seem dominated by glycinergic input and the ON cone bipolar and rod bipolar cells by GABAergic input (Grunert U, 2000451 ). The responses of most retinal ganglion cells are transient because bipolar-to-ganglion cell transmission is truncated after 150 msec by a feedback inhibition to bipolar cell terminals from GABAergic amacrine cells; the feedback inhibition itself must be delayed by approximately 150 msec to allow the initial bipolar-ganglion cell transmission.
One source of the delay appears to be glycinergic amacrine cells to GABAergic amacrine cells to bipolar cell terminals. Results suggest that, after a light flash, a population of glycinergic amacrine cells responds first, inhibiting a population of GABAergic amacrine cells for approximately 150 msec. The GABAergic amacrine cells feed back to bipolar terminals, only after the 150 msec delay, thus allowing the bipolar terminals to excite ganglion cells for the first 150 msec. (Roska and Nemeth E and Werblin FS, 1998452 ). |
| amacrine | Glycine |
| Depolarization induced transient outward currents that resembled IPSCs and were blocked by GABA and glycine receptor antagonists, suggesting that they arise from activation of amacrine feedback synapses (Protti DA and Llano I, 1998378 ). The OFF cone bipolar cells seem dominated by glycinergic input and the ON cone bipolar and rod bipolar cells by GABAergic input (Grunert U, 2000451 ). |
| presynaptic receptors | mGluR |
| Group III mGluRs mediate a direct suppression of bipolar cell transmitter release, through a mechanism of presynaptic autoreceptors (Awatramani GB and Slaughter MM, 2001394 ). |
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