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G.–L. Li, J. Vigh, H. von Gersdorff; Short–Term Depression of the Reciprocal Synapses Between Bipolar and Amacrine Cells in Goldfish Retina . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2284.
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To study the plasticity on the reciprocal synapses between the bipolar cell (BC) and amacrine cells (ACs) in goldfish retina, we applied double–pulse step stimuli to axotomized Mb BC terminals. The feedback response from the second step was depressed within the first 5 s due to the lower availability of releasable glutamate vesicles in the BC terminal, and then potentiated (after a period >1 min) due to activation of mGluR1 on amacrine cells. Here we set out to investigate the mechanism underlying the depression in the middle time range (5 s ∼ 1 min).
Whole–cell patch clamp recordings, combined with capacitance measurements to monitor glutamate release, were made directly from the axotomized Mb BC terminals in goldfish retinal slices, and double–pulse step (100 ms, from –60 to 0 mV) stimuli with variable intervals (0.5 s ∼ 1 min) were applied via the recording pipette.
Our results showed that glutamate release (induced by 100 ms step to 0 mV), as measured by capacitance jump, recovered very quickly (tau ∼ 2 s, single exponential). Therefore, we used double–pulse step with 10 s interval to study the middle time range depression. In addition, 50 microM LY 367385 was included in the bath to block the potentiation due to the mGluR1 activation. Neither blockade of NMDA or AMPA receptor had any effect on the depression, indicating it was not associated specifically with any of the two types of glutamate receptors on ACs. However, with fast application system on excised outside–out patches pulled from BC terminals, we found that the recovery of GABAA receptors from desensitization ranged from several hundred millisecond to half a minute, depending how long these receptors have seen GABA. Nevertheless, in the slice in the presence of 100 microM bicuculline, the depression of reciprocal feedback response (mediated by GABAC receptors) was unaffected, indicating that desensitization of GABAA receptors itself cannot account for the depression.
Both the replenishment of synaptic vesicles in GABAergic ACs and the desensitization of GABAA receptors on the BC terminal may contribute to the middle time range depression (5 s ∼ 1 min) on the reciprocal synapses.
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