Artificial Vision: Vision of a Newcomer - Artificial Sight: Basic Research, Biomedical Engineering, and Clinical Advances - page 41

Figure 2.5. Protection of retinal ganglion cells (RGCs) by transcorneal electrical stimu-
lation (TES). The RGCs were labeled by fluorescent dye retrogradely from bilateral
superior colliculi before optic nerve transection. A biphasic pulse of 100A was applied
through corneal lens-type electrode for an hour after the transection of rat optic nerve.
With this current, the EEP was effectively recorded from the SC of the intact rat in
other experiment, suggesting that retina was stimulated enough by the current through the
contact lens electrode. One week after optic nerve transection, the surviving RGCs were
counted. The photomicrographs of the flat-mounted retinas shows more RGCs survived
in 'cut + TES' retina than 'cut' retina with transection only. In the sham operated group,
53% of RGCs survived, while 'cut + TES' group showed 70-85% survival. This proved
that the electrical stimulation on the retina was effective to promote the survival of RGCs.
Intact, the intact retina; cut, the retina with optic nerve transection; sham, the retina with
optic nerve transection and attachment of TES electrode but without current through it;
cut + TES, the retina with optic nerve transection and TES.
indicate that IGF-1 plays a key role in the TES-induced neuroprotection of the
axotomized RGCs.
To investigate in more detail the mechanism of the neural protection, the
localization of IGF-1 in the retina after TES was examined immunohistologically
(Figure 2.7). In the normal retina, IGF-1 was present only in the inner limiting
membrane (ILM) and the nerve fiber layer. After TES, the IGF-1 immunore-
activity expanded from the ILM to the inner nuclear layer (INL) on day 7. An
especially intense signal was observed from the radial structure extending from
INL to ILM. The double staining of IGF-1 and glutamine synthetase, a marker
of Müller cells, showed that the IGF-1 signal was strong on the endfeet and
processes of the Müller cells, in addition to the diffuse signals in the inner retina.
These immunohistological results showed that Müller cells produced IGF-1 after
TES and release it into the extracellular space. Although it remains to be resolved
whether activation of RGCs itself is required for neuroprotection by TES and the
mechanism of activation of the Müller cells by TES, these series of experiments