advertisement

Editors Selection IGR 7-3

Comments

Comment by Leonard A. Levin on:

23848 Axonal regeneration induced by repetitive electrical stimulation of crushed optic nerve in adult rats, Tagami Y; Kurimoto T; Miyoshi T et al., Japanese Journal of Ophthalmology, 2009; 53: 257-266

Find related abstracts

Maintaining physiological levels of electrical activity is important forretinal ganglion cell (RGC) survival. In the normal retina, blockingelectrical activity decreases RGC responsiveness to trophic survivalsignals, and after axon injury in the optic nerve, providing RGCs withextra electrical stimulation enhances trophic responsiveness and survival(Neuron 23: 285). The mechanisms for this phenomenon arestill being explored, but the observation provides an important clinicalapproach to RGC neuroprotection in optic neuropathies. In thismanuscript, Tagami et al. extend their prior work using corneal electrodeson adult rats to electrically stimulate the retina. They previouslyshowed that transcorneal electrical stimulation (TES) enhancesRGC survival after optic nerve injury (IOVS 46: 2147), and here theydemonstrate that the same treatment enhances RGC axon regenerationinto the optic nerve. These data are consistent with priordata from RGC cultures, in which axon growth in vitro is greatlyenhanced by physiologic levels of electrical activity (Neuron 33: 689).In vivo, the effects are dose-dependent, with increasing axon growthin response to increasing doses of TES. The effect is only seenat 250 microns, however, with no additional growth even as faras 0.5 mm, suggesting that the stimulation is only enhancingshort-range sprouting, not long-range growth.
It will be exciting to see whether combining TES with a complementaryapproach � for example, providing exogenous growth factors likeCNTF, or blocking glial-associated growth inhibitors � would moregreatly promote survival and axon growth. Interestingly, this grouphas previously published on the ability of TES to stimulate phosphenesensation in human eyes, with a minimum of documented toxicity(JJO 50: 266). Thus there is strong motivation and justificationto consider TES for well-designed human clinical trials.

• ← Previous
• Next →