scholarly journals Retinal Ganglion Cell Loss in a Rat Ocular Hypertension Model Is Sectorial and Involves Early Optic Nerve Axon Loss

2011 ◽  
Vol 52 (1) ◽  
pp. 434 ◽  
Author(s):  
Ileana Soto ◽  
Mary E. Pease ◽  
Janice L. Son ◽  
Xiaohai Shi ◽  
Harry A. Quigley ◽  
...  
2012 ◽  
Vol 9 (1) ◽  
Author(s):  
Roberta Brambilla ◽  
Galina Dvoriantchikova ◽  
David Barakat ◽  
Dmitry Ivanov ◽  
John R Bethea ◽  
...  

1993 ◽  
Vol 24 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Maria-Paz Villegas-Pérez ◽  
Manuel Vidal-Sanz ◽  
Michael Rasminsky ◽  
Garth M. Bray ◽  
Albert J. Aguayo

2015 ◽  
Vol 56 (8) ◽  
pp. 4487 ◽  
Author(s):  
Giuseppe Rovere ◽  
Francisco M. Nadal-Nicolás ◽  
Marta Agudo-Barriuso ◽  
Paloma Sobrado-Calvo ◽  
Leticia Nieto-López ◽  
...  

2021 ◽  
Vol Volume 14 ◽  
pp. 6857-6869
Author(s):  
Qianxue Mou ◽  
Ke Yao ◽  
Meng Ye ◽  
Bowen Zhao ◽  
Yuanyuan Hu ◽  
...  

2019 ◽  
Author(s):  
Ashish Bhandari ◽  
Jennie C. Smith ◽  
Yang Zhang ◽  
Lisa Reid ◽  
Toni Goeser ◽  
...  

AbstractAxonopathy is a hallmark of many neurodegenerative diseases including glaucoma, where elevated intraocular pressure (ocular hypertension, OHT) stresses retinal ganglion cell (RGC) axons as they exit the eye and form the optic nerve. OHT causes early changes in the optic nerve such as axon atrophy, transport inhibition, and gliosis. Importantly, many of these changes appear to occur prior to irreversible neuronal loss, making them promising points for early diagnosis of glaucoma. It is unknown whether OHT has similarly early effects on the function of RGC output to the brain. To test this possibility, we elevated eye pressure in mice by anterior chamber injection of polystyrene microbeads. 5 weeks post-injection, bead-injected eyes showed a modest RGC loss in the peripheral retina, as evidenced by RBPMS antibody staining. Additionally, we observed reduced dendritic complexity and lower spontaneous spike rate of On-αRGCs, targeted for patch clamp recording and dye filling using a Opn4-cre reporter mouse line. To determine the influence of OHT on retinal projections to the brain, we expressed Channelrhodopsin-2 (ChR2) in melanopsin-expressing retinal ganglion cells by crossing the Opn4-cre mouse line with a ChR2-reporter mouse line and recorded post-synaptic responses in thalamocortical relay neurons in the dorsal lateral geniculate nucleus (dLGN) of the thalamus evoked by stimulation with 460 nm light. The use of a Opn4-cre reporter system allowed for expression of ChR2 in a narrow subset of RGCs responsible for image-forming vision in mice. Five weeks following OHT induction, paired pulse and high-frequency stimulus train experiments revealed that presynaptic vesicle release probability at retinogeniculate synapses was elevated. Additionally, miniature synaptic current frequency was slightly reduced in brain slices from OHT mice and proximal dendrites of post-synaptic dLGN relay neurons, assessed using a Sholl analysis, showed a reduced complexity. Strikingly, these changes occurred prior to major loss of RGCs labeled with the Opn4-Cre mouse, as indicated by immunofluorescence staining of ChR2-expressing retinal neurons. Thus, OHT leads to pre- and post-synaptic functional and structural changes at retinogeniculate synapses. Along with RGC dendritic remodeling and optic nerve transport changes, these retinogeniculate synaptic changes are among the earliest signs of glaucoma.


2010 ◽  
Vol 90 (1) ◽  
pp. 168-183 ◽  
Author(s):  
Manuel Salinas-Navarro ◽  
Luis Alarcón-Martínez ◽  
Francisco J. Valiente-Soriano ◽  
Manuel Jiménez-López ◽  
Sergio Mayor-Torroglosa ◽  
...  

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