Functional changes and differential cell death of retinal ganglion cells after injury

2007 ◽  
Author(s):  
Suk-yee Li
Keyword(s):  
Cell Death ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Functional Changes ◽  
Differential Cell

Low dosage chloroquine protects retinal ganglion cells against glutamate-induced cell death

2019 ◽  
Vol 181 ◽  
pp. 285-293 ◽  
Author(s):  
Xiaoyun Ma ◽  
Yun Zhang ◽  
Dan Zhu ◽  
Zufeng Chen ◽  
Manshan Xu ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Low Dosage

Neuroprotection by GH against excitotoxic-induced cell death in retinal ganglion cells

2016 ◽  
Vol 234 ◽  
pp. 68-80 ◽  
Author(s):  
Carlos G. Martínez-Moreno ◽  
José Ávila-Mendoza ◽  
Yilun Wu ◽  
Elvira del Carmen Arellanes-Licea ◽  
Marcela Louie ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion

scholarly journals Protection of Retinal Ganglion Cells from Natural and Axotomy-Induced Cell Death in Neonatal Transgenic Mice Overexpressing bcl-2

1996 ◽  
Vol 16 (13) ◽  
pp. 4186-4194 ◽  
Author(s):  
Lidia Bonfanti ◽  
Enrica Strettoi ◽  
Sabrina Chierzi ◽  
Maria Cristina Cenni ◽  
Xiu-Huai Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Transgenic Mice ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion

Microglia mediate non‐cell‐autonomous cell death of retinal ganglion cells

Glia ◽  
2018 ◽  
Vol 66 (11) ◽  
pp. 2366-2384 ◽  
Author(s):  
Akiko Takeda ◽  
Youichi Shinozaki ◽  
Kenji Kashiwagi ◽  
Nobuhiko Ohno ◽  
Kei Eto ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion

Hypothermia protects retinal ganglion cells against hypoxia‐induced cell death in a retina organ culture model

2019 ◽  
Vol 47 (8) ◽  
pp. 1043-1054 ◽  
Author(s):  
Patricia Klemm ◽  
José Hurst ◽  
Matthias Dias Blak ◽  
Thoralf Herrmann ◽  
Marion Melchinger ◽  
...  
Keyword(s):  
Cell Death ◽  
Organ Culture ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Culture Model

Retinal Ganglion Cells Functional Changes in a Mouse Model of Alzheimer’s Disease Are Linked with Neurotransmitter Alterations

2021 ◽  
pp. 1-14
Author(s):  
Joaquín Araya ◽  
Felipe Bello ◽  
Gaganashree Shivashankar ◽  
David Neira ◽  
Claudia Durán-Aniotz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Firing Rate ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Gamma Aminobutyric Acid ◽  
Functional Changes ◽  
Model Of Alzheimer’S Disease

Background: Alzheimer’s disease (AD) is the most prevalent form of dementia worldwide. This neurodegenerative syndrome affects cognition, memory, behavior, and the visual system, particularly the retina. Objective: This work aims to determine whether the 5xFAD mouse, a transgenic model of AD, displays changes in the function of retinal ganglion cells (RGCs) and if those alterations are correlated with changes in the expression of glutamate and gamma-aminobutyric acid (GABA) neurotransmitters. Methods: In young (2–3-month-old) and adult (6-7-month-old) 5xFAD and WT mice, we have studied the physiological response, firing rate, and burst of RGCs to various types of visual stimuli using a multielectrode array system. Results: The firing rate and burst response in 5xFAD RGCs showed hyperactivity at the early stage of AD in young mice, whereas hypoactivity was seen at the later stage of AD in adults. The physiological alterations observed in 5xFAD correlate well with an increase in the expression of glutamate in the ganglion cell layer in young and adults. GABA staining increased in the inner nuclear and plexiform layer, which was more pronounced in the adult than the young 5xFAD retina, altering the excitation/inhibition balance, which could explain the observed early hyperactivity and later hypoactivity in RGC physiology. Conclusion: These findings indicate functional changes may be caused by neurochemical alterations of the retina starting at an early stage of the AD disease.

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