【摘 要】
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Objective:bipolar cells (BCs) commu-nicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses.Reconstructing the published quantita-tive release data from electrical soma stimulation
【机 构】
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Institute for Analysis and Scientific Computing,Vienna University of Technology,Wiedner Hauptstrasse
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Objective:bipolar cells (BCs) commu-nicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses.Reconstructing the published quantita-tive release data from electrical soma stimulation (voltage clamp experiments) of rat rod BCs were used to develop two simple models to predict the number of released vesi-cles as time series.In the experiment,the currents coming to the AII amacrine cell originating from releasing vesicles from the rod BC were recorded using paired-recordings in whole-cell voltage-clamp method.Method:one of the models is based directly on terminal transmembrane volt-age,so-called \'modelV\',whereas the temporally exacter modelCa includes changes of intracellular calcium con-centrations at terminals.Result:the intracellular calcium concentration method replicates a 0.43 ms signal delay for the transient release to pulsatile stimulation as a con-sequence of calcium channel dynamics in the presynaptic membrane,while the modelV has no signal delay.Both models produce the quite similar results in low stimuli amplitudes.However,for large stimulation intensities that may be done during extracellular stimulations in retinal implants,the modelCa predicts that the reversal potential of calcium limits the number of transiently released ves-icles.Adding sodium and potassium ion channels to the axon of the cell enable to study the impact of spikes on the transient release in BC ribbons.Conclusion:a spike elicited by somatic stimulation causes the rapid release of all vesicles that are available for transient release,while a non-spiking BC with a similar morphometry needs stronger stimuli for any transient vesicle release.During extracellular stimulation,there was almost no difference in transient release between the active and passive cells because in both cases the terminal membrane of the cell senses the same potentials originating from the micro-electrode.An exception was found for long pulses when the spike has the possibility to generate a higher termi-nal voltage than the passive cell.Simulated periodic 5 Hz stimulation showed a reduced transient release of 3 vesi-cles per stimulus,which is a recovery effect.
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