Reduced Dendritic Spines in the Visual Cortex Contralateral to the Optic Nerve Crush Eye in Adult Mice

Abstract

Purpose To determine alteration of dendritic spines and associated changes in the primary visual cortex (V1 region) related to unilateral optic nerve crush (ONC) in adult mice. Methods Adult unilateral ONC mice were established. Retinal nerve fiber layer (RNFL) thickness was measured by spectral-domain optical coherence tomography. Visual function was estimated by flash visual evoked potentials (FVEPs). Dendritic spines were observed in the V1 region contralateral to the ONC eye by two-photon imaging in vivo. The neurons, reactive astrocytes, oligodendrocytes, and activated microglia were assessed by NeuN, glial fibrillary acidic protein, CNPase, and CD68 in immunohistochemistry, respectively. Tropomyosin receptor kinase B (TrkB) and the markers in TrkB trafficking were estimated using western blotting and co-immunoprecipitation. Transmission electron microscopy and western blotting were used to evaluate autophagy. Results The amplitude and latency of FVEPs were decreased and delayed at 3 days, 1 week, 2 weeks, and 4 weeks after ONC, and RNFL thickness was decreased at 2 and 4 weeks after ONC. Dendritic spines were reduced in the V1 region contralateral to the ONC eye at 2, 3, and 4 weeks after ONC, with an unchanged number of neurons. Reactive astrocyte staining was increased at 2 and 4 weeks after ONC, but oligodendrocyte and activated microglia staining remained unchanged. TrkB was reduced with changes in the major trafficking proteins, and enhanced autophagy was observed in the V1 region contralateral to the ONC eye. Conclusions Dendritic spines were reduced in the V1 region contralateral to the ONC eye in adult mice. Reactive astrocytes and decreased TrkB may be associated with the reduced dendritic spines.

Mesoscopic cortical network reorganization during recovery of optic nerve injury in GCaMP6s mice

“…The visual cortex is at first inactivated by the lack of retinal input and related impairment 19 , similar to the decrease in brain function following optic neuritis, which is proportional to the extent of the damage of the optic nerve [20][21][22] . These results are in line with recent findings showing cortical plasticity in V1 after an ONC in rats or mice 10,[23][24][25][26] followed by a recovery of cortical activity. This recovery is in agreement with previous autoradiographic studies after an ONC in rats 27 .…”

Mettl14-mediated m6A modification modulates neuron apoptosis during the repair of spinal cord injury by regulating the transformation from pri‐mir‐375 to miR-375

“…2g), suggesting that shRNA-Mettl14 is helpful to stabilize microtubule structure and repair neurites. Axonal regeneration is beneficial to the recovery of motor function of hind limbs in rats with spinal cord defect, and the scar caused by astrocytes at the edge of injury will hinder axonal regeneration; NeuN, GFAP and NF-200 are used to evaluate neuronal, axonal regeneration and glial scab formation in the spinal cord [19,20]. Then, to determine whether shRNA-Mettl14 affects the repair of spinal cord defect, we detected the positive expression of GFAP, NeuN and NF-200 by immunohistochemistry.…”

Human umbilical cord mesenchymal stem cells-derived extracellular vesicles facilitate the repair of spinal cord injury via the miR-29b-3p/PTEN/Akt/mTOR axis

“…3A ; all p < 0.001). NeuN, GFAP, and NF-200 represent neurons, axon regeneration, and glial scab formation in the spinal cord [ 21 , 22 ]. The number of NeuN was decreased significantly in SCI rats but increased in the EVs-treated rats (Fig.…”