XXXX currents and @entity460 signaling in rod bipolar cells of @entity35 retinal slices.

@entity1246 @entity2228 @entity141 @entity4524 @entity460 @entity594 @entity35 @entity4768 @entity9898
Combined electrophysiological and imaging techniques were used to study @entity460 currents (ICa) and their sites of origin at rod bipolar cells in @entity35 retinal slices. We report here for the first time the successful whole-cell patch-clamp recording from presynaptic boutons that were compared with somatic recordings. @entity4524 -resistant inward currents were elicited in response to depolarization. The kinetic and pharmacological properties of ICa were very similar for recordings obtained from the soma and the presynaptic terminals. ICa activated maximally between -30 and -20 mV was enhanced by @entity9898 and was blocked by @entity4768 and @entity594 . Peak amplitude and time to peak were -31.3 +/- 1.2 pA and 3.2 +/- 0.2 msec with somatic recordings (n = 54), whereas the corresponding values were -31.6 +/- 6.1 pA and 3.2 +/- 0.7 msec in recordings obtained directly from terminals (n = 6). ICa showed little inactivation during sustained depolarizations. No T-type ICa was observed with depolarizations from -90 mV. Concomitant with @entity141 entry, depolarization induced the appearance of transient outward currents that resembled IPSCs and were blocked by @entity1246 and @entity2228 receptor antagonists, suggesting that they arise from activation of amacrine feedback synapses. Upon depolarization, intracellular @entity141 ([ @entity141 ]i) rises were restricted to the presynaptic terminals with no somatic or axonal changes and were linearly dependent on pulse duration when using a low-affinity @entity141 indicator. In cone bipolar cells, ICa inactivated markedly, and [ @entity141 ]i rises occurred in the axon, as well as in the presynaptic terminals.
