Different patterns of changes between actin dynamics and synaptic density in the rat’s primary visual cortex during a special period of visual development

Chen, Mei-Qing; Bi, Ai-Ling; Zhang, Yueying; Yan, Qi; Sun, Yuanyuan; Zhang, Xiuyan; Ma, Xianzhen; Bi, Hongsheng

doi:10.1016/j.brainresbull.2017.06.004

Cited by 4 publications

(11 citation statements)

References 33 publications

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“…While the critical period for ODP is commonly associated with synapse pruning, previous studies have not consistently observed decreases in dendritic spine densities during this time 5,7,47 . This inconsistency is likely due to variability in methods of spine counting, the types of dendrites analyzed, the ages of animals assayed, the laminar locations of neurons analyzed, or differences in model organism 5,7,47,48,55 . One study found the spine densities on apical dendrites from L2/3 and L5 visual cortical neurons were highly variable and increased slightly between P20 and P30 47 .…”

Section: Discussionmentioning

confidence: 77%

“…Neurons in visual cortex have been shown to experience intense synaptogenesis following eye opening 4,5 . This period of synapse formation (P14-P21 in mouse) is followed by the critical period for optical dominance plasticity (P21-P35), which is associated with synaptic refinement and pruning 4,7 .…”

Section: Spine Densities On Apical and Basal Dendrites Demonstrate DImentioning

confidence: 99%

“…The number and strength of synapses found on visual cortical neurons (often inferred from dendritic spine density and shape) depend on visual experience and developmental stage 3 . During the postnatal development of visual cortex, neurons experience an early increase in dendritic spine densities following eye opening 4,5 . This period of heightened synaptogenesis is followed by the critical period for ocular dominance plasticity (ODP, postnatal day (P)21-P35), which is associated with synaptic refinement and pruning 1, 3,6,7 .…”

Section: Introductionmentioning

confidence: 99%

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Precise levels of Nectin-3 and an interaction with Afadin are required for proper synapse formation in postnatal visual cortex

Tomorsky

Parker

et al. 2019

Preprint

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Developing cortical neurons must express numerous molecules to form and strengthen specific synaptic connections during circuit formation. Nectin-3 is a cell-adhesion molecule with known roles in the development and maintenance of hippocampal circuits. This protein and its binding partner, nectin-1, are selectively expressed in upper-layer neurons of mouse visual cortex, but their role in the development of cortical circuits is unknown. Here we block nectin-3 expression (via shRNA) or overexpress either full length (OE) or dominant-negative (DN, lacking a C-terminus) nectin-3 in developing layer 2/3 visual cortical neurons using in utero electroporation. We then assay dendritic spine densities at three developmental time points: eye opening (postnatal day (P)14), one week following eye opening after a period of heightened synaptogenesis (P21), and at the close of the critical period for ocular dominance plasticity (P35). shRNA knockdown of nectin-3 beginning at E15.5 or ~P19, increased dendritic spine densities at P21 or P35, respectively. Increasing nectin-3 binding/adhesion by expressing either DN nectin-3 (intact extracellular binding domain but lacking a Cterminus) or OE nectin-3 constructs beginning at E15.5, produced overall decreases in dendritic spine densities. However, DN nectin-3 expression alone prevented the increase in spine densities typically observed between P14 and P21. This suggests that nectin-3 intracellular signaling (reduced with DN expression) has a role in spine formation after eye opening. These data collectively suggest that both functional intracellular signaling and balanced overall expression of nectin-3 are required for normal synapse formation during the development of layer 2/3 visual cortical neurons.

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Section: Discussionmentioning

confidence: 77%

Section: Spine Densities On Apical and Basal Dendrites Demonstrate DImentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Precise levels of Nectin-3 and an interaction with Afadin are required for proper synapse formation in postnatal visual cortex

Tomorsky

Parker

et al. 2019

Preprint

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“…The number and strength of synapses found on visual cortical neurons, inferred from dendritic spine density and shape, depend on visual experience and developmental stage [ 1 , 12 – 19 ]. During the postnatal development of visual cortex, neurons experience an early increase in dendritic spine densities following eye opening [ 18 , 20 , 21 ]. This period of heightened synaptogenesis is followed by the critical period for ocular dominance plasticity (ODP, postnatal day (P)21 – P35), which is associated with experience-dependent synaptic refinement and pruning [ 2 , 4 , 19 , 20 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

“…During the postnatal development of visual cortex, neurons experience an early increase in dendritic spine densities following eye opening [ 18 , 20 , 21 ]. This period of heightened synaptogenesis is followed by the critical period for ocular dominance plasticity (ODP, postnatal day (P)21 – P35), which is associated with experience-dependent synaptic refinement and pruning [ 2 , 4 , 19 , 20 , 22 ]. Dendritic spine remodeling provides a mechanism for synapses to alter their strength and number based on experience, e.g.…”

Section: Introductionmentioning

confidence: 99%

Precise levels of nectin-3 are required for proper synapse formation in postnatal visual cortex

et al. 2020

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Background Developing cortical neurons express a tightly choreographed sequence of cytoskeletal and transmembrane proteins to form and strengthen specific synaptic connections during circuit formation. Nectin-3 is a cell-adhesion molecule with previously described roles in synapse formation and maintenance. This protein and its binding partner, nectin-1, are selectively expressed in upper-layer neurons of mouse visual cortex, but their role in the development of cortical circuits is unknown. Methods Here we block nectin-3 expression (via shRNA) or overexpress nectin-3 in developing layer 2/3 visual cortical neurons using in utero electroporation. We then assay dendritic spine densities at three developmental time points: eye opening (postnatal day (P)14), one week following eye opening after a period of heightened synaptogenesis (P21), and at the close of the critical period for ocular dominance plasticity (P35). Results Knockdown of nectin-3 beginning at E15.5 or ~ P19 increased dendritic spine densities at P21 or P35, respectively. Conversely, overexpressing full length nectin-3 at E15.5 decreased dendritic spine densities when all ages were considered together. The effects of nectin-3 knockdown and overexpression on dendritic spine densities were most significant on proximal secondary apical dendrites. Interestingly, an even greater decrease in dendritic spine densities, particularly on basal dendrites at P21, was observed when we overexpressed nectin-3 lacking its afadin binding domain. Conclusion These data collectively suggest that the proper levels and functioning of nectin-3 facilitate normal synapse formation after eye opening on apical and basal dendrites in layer 2/3 of visual cortex.

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Activation of p38 MAPK hinders the reactivation of visual cortical plasticity in adult amblyopic mice

Wang,

Hou,

et al. 2023

Experimental Eye Research

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Different patterns of changes between actin dynamics and synaptic density in the rat’s primary visual cortex during a special period of visual development

Cited by 4 publications

References 33 publications

Precise levels of Nectin-3 and an interaction with Afadin are required for proper synapse formation in postnatal visual cortex

Precise levels of Nectin-3 and an interaction with Afadin are required for proper synapse formation in postnatal visual cortex

Precise levels of nectin-3 are required for proper synapse formation in postnatal visual cortex

Activation of p38 MAPK hinders the reactivation of visual cortical plasticity in adult amblyopic mice

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