Differentiation of Hebbian and homeostatic plasticity mechanisms within layer 5 visual cortex neurons.
Differentiation of Hebbian and homeostatic plasticity mechanisms within layer 5 visual cortex neurons.
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DOI:
10.1016/j.celrep.2022.110892
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发表时间:
2022-05-31
期刊:
影响因子:
8.8
通讯作者:
Fox, Kevin
中科院分区:
文献类型:
--
作者:
Pandey, Anurag;Hardingham, Neil;Fox, Kevin
Cortical layer 5 contains two major types of projection neuron known as IB (intrinsic bursting) cells that project sub-cortically and RS (regular spiking) cells that project between cortical areas. This study describes the plasticity properties of RS and IB cells in the mouse visual cortex during the critical period for ocular dominance plasticity. We find that RS neurons exhibit synaptic depression in response to both dark exposure (DE) and monocular deprivation (MD), and their homeostatic recovery from depression is dependent on TNF-α. In contrast, IB cells demonstrate opposite responses to DE and MD, potentiating to DE and depressing to MD. IB cells’ potentiation depends on CaMKII-autophosphorylation and not TNF-α. IB cells show mature synaptic properties at the start of the critical period while RS cells mature during the critical period. Together with observations in somatosensory cortex, these results suggest that differences in RS and IB plasticity mechanisms are a general cortical property. Layer 5 RS cell synapses mature during critical period for ocular dominance plasticity Layer 5 RS but not IB cells show TNF-α-dependent homeostatic recovery from depression Layer 5 IB but not RS cells show CaMKII-autophosphorylation-dependent potentiation Increases in spine head size precede functional potentiation in IB cells Pandey et al. show that cells in the visual cortex projecting to different neuronal targets exhibit different synaptic plasticity mechanisms. While regular spiking (RS) cells show synaptic depression and exhibit TNF-α-dependent homeostatic recovery from depression, intrinsic bursting (IB) cells show potentiation that depends on CaMKII-autophosphorylation and not TNF-α.
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