شماره ركورد :
90089
عنوان مقاله :
قشر بينايي موش صحرايي IV اثر محروميت از بينايي روي تقويت دراز مدت ناشي از تحريك تتانيك ماده سفيد و لايه
عنوان به زبان ديگر :
Effect of Visual Deprivation on Long-term Potentiation of Layer II/III Responses Triggered by Tetanic Stimulation of White Matter and Layer IV of the Rat Visual Cortex
پديد آورندگان :
محمود سلامي زواره ، مترجم ,
رتبه نشريه :
-
تعداد صفحه :
9
از صفحه :
129
تا صفحه :
137
كليدواژه :
dark rearing , layer IV , LTP , ماده سفيد , white matter , محروميت از بينايي , LTP , IV لايه , PBS , PBS
چكيده لاتين :
Long-term potentiation (LTP) is a dominated mechanism of learning and memory in the hippocampus and neocortex. In the neocortex environmental signals may underlie LTP. In this study we investigated the effects of dark rearing on potentiation of layer II/III responses to stimulation of layer IV or the underlying white matter in the visual cortex in vitro. LTP was induced by primed-burst stimulation (PBs) applied to white matter or layer IV of the cortex in light and dark reared rats. Regardless of the stimulation site, layer II/III field potentials consisted of two excitatory postsynaptic potentials (EPSP) named EPSP1 and EPSP2. In general, latency of responses in dark reared rats was shorter than that in light reared ones. Whereas PBs of layer IV produced LTP of two components in both groups, that of white matter induced an appreciable potentiation of EPSP2 in both groups and EPSP1 in dark reared rats. These results indicate that PBs of either white matter or layer IV can gain access to the modifiable synapses that are related to EPSP2 of layer II/III responses in light and dark reared visual cortex, but accessibility of the modifiable synapses that are related to EPSP1 depends on tetanization site. The dark rearing enhances accessibility of the modifiable synapses that are related to EPSP1 following PBs of the white matter. It is suggested that the immaturity of inhibitory circuits and/or better function of excitatory ones in the visual cortex of dark reared rats may contribute to the enhanced accessibility of EPSP1.
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