Biology Reference
In-Depth Information
with the reported effects of electrical stimulations on the survival and axonal
elongation of axotomized motoneurons in the rat spinal cord (
Al-Majed,
Brushart, et al., 2000
).
Goldberg et al. (2002)
reported that when cultured
rat RGCs were continuously stimulated with electrical pulses, the number
of surviving RGCs increased by 10-fold over the control values.
Transcorneal electrical stimulation (TES), which is less invasive than elec-
trical stimulationof theON, also increased the survival ofRGCs afterONtran-
section
in vivo
by upregulating endogeneous IGF-1 (
Morimoto et al., 2005
).
TES also increased axonal preservation over the unstimulated controls after
crushing the ON (
Miyake, Yoshida, Inoue, & Hata, 2007
). TES enhanced
the axonal regeneration of RGCs through the activation of the IGF-1 pathway
in the rat ON crush model (
Tagami et al., 2009
). Similarly in animals with
inherited photoreceptor degeneration, TES enhanced the survival of the pho-
toreceptors in Royal College of Surgeons (RCS) rats (
Morimoto et al., 2007
),
P347L transgenic rabbits (
Morimoto et al., 2012
), and rats exposed to excessive
light stimulation, that is, phototoxicity (
Ni,Gan,Xu,Xu,&Da,2009
). TES
also had neuroprotective effects on ischemic damaged retinas
in vivo
(
Wang
et al., 2011
). TES enhanced the survival of retinal neurons by increasing various
neurotrophic factors: IGF-1 (
Morimoto et al., 2005
), BDNF (
Ni et al., 2009
),
and other neuroprotective factors (
Willmann et al., 2011
).
Thus, the results of several animal studies clearly showed a neuro-
protective effect of TES in eyes with degenerative retinal diseases and in eyes
with optic neuropathies.
The results of TES have been published for patients with nonarteritic anterior
ischemic and traumatic optic neuropathy (
Fujikado et al., 2006
), retinal artery
occlusion (
Inomata et al., 2007
), and retinal vein occlusion (
Oono et al.,
2011
). A controlled, randomized study in patients with RP has been recently
published where positive tendencies and statistically significant improvements
in visual functionwere observed in one subgroup of patients (
Schatz et al., 2011
).
A retinal prosthesis is a type of neuroprosthesis. A subretinal implant of an
artificial retina can stimulate the retina electrically and has a neuroprotective
effect on the photoreceptors of RCS rats (
Pardue et al., 2005
) and the retinal
function in patients (
Chow, Bittner, & Pardue, 2010
). Subretinal electrical
stimulation by a subretinal implant can enhance the visual function in areas
distant from the implant which has been attributed to an upregulation in the
expression of neurotrophic factors such as fibroblast growth factor-2
(FGF-2) in an activity-dependent fashion (
Ciavatta et al., 2009
). Electrical
stimulation also improves the survival of cells in the inner retinal layers, for
example, the amacrine and bipolar cells, in explanted rat retinas in the RCS
model of retinal degeneration (
Schmid, Herrmann, Kohler, & Stett, 2009
).
