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Kanxing Zhao, Xuefeng Shi; In Vivo Whole-Cell Recording Reveals Rapid Heterosynaptic Response Depression of Binocular Cells in Rat Visual Cortex Induced by Repeated Monocular Visual Stimulation. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3904.
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© ARVO (1962-2015); The Authors (2016-present)
Recent studies show that, in addition to the rapid response depression of the deprived eye, monocular deprivation (MD) also induces a delayed open-eye potentiation. However, whether the imbalance of binocular inputs could also result in this heterosynaptic response alteration in non-MD conditions is still unclear. Here we investigated the changes of visually evoked response of rat binocular visual cortical cells to one eye after intensively repeated monocular stimulation of the contralateral eye.
We performed in vivo whole-cell patch-clamp recordings in binocular visual cortical cells of normally reared rats at 6-8 postnatal weeks. Receptive field mapping and baseline monocular response measurement were done for each eye before intensively visual stimulation of one eye, during which no any stimulation was exerted on the other eye. We measured the visually evoked responses of the binocular cells to both eyes, respectively, at 60min after stimulation. Only cells with stable input resistances during recording period were included for analysis.
Subthreshold excitatory postsynaptic potentials (EPSPs) and excitatory postsynaptic currents (EPSCs) were evoked by visual stimulation. After repeated monocular visual stimulation of one eye, the EPSPs and EPSCs of the cells to the other eye were significantly depressed (P<0.05). However, no homosynaptic potentiation of responses to the intensively stimulated eye in these cells were observed at 60min after stimulation (P>0.05).
We directly showed that the reinforced visual stimulation of one eye rapidly depresses the synaptic inputs from the other eye, but homosynaptic potentiation can’t be induced in the early phase of experience-dependent visual plasticity in the in-vivo condition. This binocular-input-imbalance induced heterosynaptic plasticity may shed light on the mechanism of binocular competitive interaction and homeostatic regulation of neural circuits.
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