Topographic Quantification of the Transcorneal Electrical Stimulation (TES)-Induced Protective Effects on N-Methyl-N-Nitrosourea-Treated Retinas.
To quantify the transcorneal electrical stimulation (TES)-induced effects on regional photoreceptors and visual signal pathway of N-methyl-N-nitrosourea (MNU)-treated retinas via topographic measurements.



N-methyl-N-nitrosourea-administered mice received TES or sham stimulations and were subsequently subjected to electroretinography (ERG), multielectrode array (MEA), and histologic and immunohistochemistry examinations. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analyses were also performed to determine the mRNA levels of Bax, Bcl-2, Calpain-2, Caspase-3, brain-derived neurotrophic factor (BDNF), and ciliary neurotrophic factor (CNTF).



Amplitudes of ERG b-wave in the TES-treated mice were significantly larger than those in the sham controls (P < 0.01). Microelectrode array examination revealed that the photoreceptors in TES-treated retina were efficiently preserved (P < 0.01). Morphologic measurements showed that the central retina region was more consolidated than the other areas in the TES-treated mice. Together with the disproportionate distribution of immunostaining in retinal flat mounts, these findings indicated that different rescuing kinetics existed among regional photoreceptors. Compared with the sham controls, a significantly increased signal-to-noise ratio was also found in the TES-treated mice (TES100: 2.02 ± 1.12; TES200: 4.42 ± 1.51; sham: 0.25 ± 0.13; P < 0.01). Moreover, qRT-PCR measurements suggested that the altered expression of several apoptotic factors and neurotrophic cytokines was correlated with TES-induced protection.



Regional photoreceptors in the MNU-administered retinas exhibit different sensitivities to TES. Transcorneal electrical stimulation is capable of ameliorating MNU-induced photoreceptor degeneration and rectifying abnormalities in the inner visual signal pathways.
Department of Ophthalmology, General Hospital of Chinese PLA, Ophthalmology & Visual Science Key Lab of PLA, Beijing, People's Republic of China.
Ye
Y
Tao
Department of Clinical Aerospace Medicine, Fourth Military Medical University, Xi'an, People's Republic of China.
Tao
T
Chen
Department of Gynaecology & Obstetrics, General Hospital of Chinese PLA, Beijing, People's Republic of China.
Zhong-Yu
ZY
Liu
Department of Ophthalmology, General Hospital of Chinese PLA, Ophthalmology & Visual Science Key Lab of PLA, Beijing, People's Republic of China.
Li-Qiang
LQ
Wang
Department of Ophthalmology, General Hospital of Chinese PLA, Ophthalmology & Visual Science Key Lab of PLA, Beijing, People's Republic of China.
Wei-Wei
WW
Xu
Department of Ophthalmology, General Hospital of Chinese PLA, Ophthalmology & Visual Science Key Lab of PLA, Beijing, People's Republic of China.
Li-Min
LM
Qin
Department of Ophthalmology, General Hospital of Chinese PLA, Ophthalmology & Visual Science Key Lab of PLA, Beijing, People's Republic of China.
Guang-Hua
GH
Peng
Department of Ophthalmology, General Hospital of Chinese PLA, Ophthalmology & Visual Science Key Lab of PLA, Beijing, People's Republic of China.
Huang
H
Yi-Fei
D000477:Alkylating Agents / Q000494:pharmacology; D000818:Animals; D003315:Cornea; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004596:Electroretinography; D005260:Female; D007150:Immunohistochemistry; D008297:Male; D008770:Methylnitrosourea / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D020419:Photoreceptor Cells, Vertebrate / Q000187:drug effects / Q000473:pathology*; D012160:Retina / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D012162:Retinal Degeneration / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*
D000477:Alkylating Agents; D008770:Methylnitrosourea