378. Protti DA and Llano I. (1998) Calcium currents and calcium signaling in rod bipolar cells of rat retinal slices. J Neurosci 18:3715-24.

NeuronCompartmentPropertyConnectivityNotes
Retina bipolar cellAxon terminalGlycineamacrineDepolarization 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 (Grünert U, 2000451 ).
Retina bipolar cellAxon terminalGabaamacrineThe 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 (Grünert 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 B et al, 1998452 ).
Retina bipolar cellAxon terminalI L high threshold.High-voltage-activated (HVA) and low-voltage-activated (LVA) Ca2+ currents were observed in the isolated rod bipolar cell terminal recordings(Pan ZH, 2001374 ). Whole-cell patch-clamp recording of ICa from presynaptic boutons are comparable to that obtained from somatic recordings, but elevation of intracellular Ca is restricted to the presynaptic terminals, with no somatic or axonal changes observed (Protti DA and Llano I, 1998378 ). L-type ICa was found only in cells that retained axon terminals ramifying in the inner plexiform layer(de la Villa P et al, 1998388 ) Hartveit E, 1999503 .

References
378. Protti DA and Llano I. (1998) Calcium currents and calcium signaling in rod bipolar cells of rat retinal slices. J Neurosci 18:3715-24.
451. Grünert U. (2000) Distribution of GABA and glycine receptors on bipolar and ganglion cells in the mammalian retina. Microsc Res Tech 50:130-40 [Journal] .
384. Tachibana M and Kaneko A. (1988) Retinal bipolar cells receive negative feedback input from GABAergic amacrine cells. Vis Neurosci 1:297-305.
452. Roska B, Nemeth E and Werblin FS. (1998) Response to change is facilitated by a three-neuron disinhibitory pathway in the tiger salamander retina. J Neurosci 18:3451-9.
374. Pan ZH. (2001) Voltage-activated Ca2+ channels and ionotropic GABA receptors localized at axon terminals of mammalian retinal bipolar cells. Vis Neurosci 18:279-88.
388. de la Villa P, Vaquero CF and Kaneko A. (1998) Two types of calcium currents of the mouse bipolar cells recorded in the retinal slice preparation. Eur J Neurosci 10:317-23.
503. Hartveit E. (1999) Reciprocal synaptic interactions between rod bipolar cells and amacrine cells in the rat retina. J Neurophysiol 81:2923-36.
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