2011 Fiscal Year Final Research Report
Mechanisms of reorganization in mouse superior colliculus after visual cortical lesions
| Project/Area Number |
22700419
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Hokkaido University |
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Principal Investigator |
KANEDA Katsuyuki 北海道大学, 大学院・薬学研究院, 准教授 (30421366)
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| Project Period (FY) |
2010 – 2011
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| Keywords | 上丘 / GABA作動性ニューロン / 局所神経回路 / 皮質視覚野損傷 / シナプス可塑性 |
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| Research Abstract |
Numerous studies have investigated the effects of lesions of the primary visual cortex(V1) on visual responses in neurons of the superficial layer of the superior colliculus(sSC), which receives visual information from both the retina and the V1. However, little is known about the changes in local circuit dynamics of the sSC after receiving V1 lesions. Here, we show that surround inhibition of sSC neurons is transiently enhanced following V1 lesions in mice and that this enhancement may be attributed to alterations in the balance between excitatory and inhibitory inputs to sSC neurons. Extracellular recordings in vivo revealed that sSC neuronal responses to large visual stimuli were transiently reduced about 1 week after visual cortical lesions compared with normal mice and that this reduction was partially recovered about 1 month after the lesions. To investigate local circuit mechanisms underlying this reduction, we performed whole-cell patch-clamp recordings from sSC neurons in slice preparations obtained from mice that had received visual cortical lesions 1 week prior to the recordings. We found cell type-dependent changes in the balance between excitation and inhibition : in non-GABAergic cells, inhibition predominated over excitation, whereas the excitation-inhibition balance did not change in GABAergic neurons. These results suggest that enhanced inhibition may be partially responsible for the reduced responses to large visual stimuli in some cells and raise the possibility that the enhanced inhibition may prevent hyperexcitability in the sSC local circuit shortly after the visual cortical lesion.
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