REVIEW: An approach for neuroprotective therapies of secondary brain damage after excitotoxic retinal injury in mice.
BACKGROUND
Many current therapeutic strategies for several eye diseases, such as glaucoma, retinal ischemia, and optic neuropathy, are focused on protection of the retinal ganglion cells (RGCs). In fact, loss of visual field, including irreversible blindness, is caused by RGC damage in these diseases. However, recent evidence suggests that the RGC damage extends to visual center in brain: the visual impairment induced by these diseases may result not only from RGC loss, but also from neuronal degeneration within the visual center in brain.


OBJECTIVE
To protect neurons within the visual center in the brain, as well as retinal treatment, for the prevention of visual disorder in these diseases.


METHODS
Once considered difficult to study the visual center in brain following RGCs loss, because obtaining the human samples that are suitable for the study may be difficult. In addition, the monkey, mainly used as glaucomatous model, is relatively high cost and needs to long experiment-span. Here, we focused on mice, because of their high degree of availability, relatively low cost, and amenability to experimental and genetic manipulation.


CONCLUSIONS
In this review, we describe time-dependent alterations in the visual center in brain following RGCs loss, and whether some drugs prevent the neuronal damage of the visual center in the brain.
Ito
Yasushi
Y
Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Japan.
Shimazawa
Masamitsu
M
Hara
Hideaki
H
D000818:Animals; D001930:Brain Injuries / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D012164:Retinal Diseases / Q000150:complications*; D011984:Sensory Receptor Cells / Q000187:drug effects; D014794:Visual Fields / Q000187:drug effects
D018696:Neuroprotective Agents