Editors' ChoiceNeuroscience

When Light Gets On Your Nerves

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Science Translational Medicine  08 Jun 2011:
Vol. 3, Issue 86, pp. 86ec86
DOI: 10.1126/scitranslmed.3002720

The 20 million Americans with peripheral nerve injury have little hope for recovery. Therapy usually consists of surgical repair (when possible) or rehabilitation focused on retraining the injured limb. But what if the problem lies not just in communication through the nerve, but communication within the brain? In a recent article, Li and colleagues demonstrated in rodents that the somatosensory cortex (S1) deprived of input by an experimental nerve injury becomes further suppressed by the normal S1 in the other hemisphere. Using optogenetic techniques, they showed that inhibiting the healthy side of the brain actually helped increase activity on the deprived side.

First, the investigators used a retrovirus to express halorhodopsin—a chloride channel that hyperpolarizes and inhibits neuronal firing when exposed to light—in the brains of rats with or without excision of the radial, median, and ulnar nerves in the forepaw. Second, they created a window to the brain by thinning the skull over the region of S1. Third, they delivered light to the healthy S1 (inhibiting the cells expressing halorhodopsin) and electrically stimulated the intact forepaw. Electrophysiological recordings of individual neurons and groups of neurons in the deprived S1 demonstrated an increase in firing when the healthy S1 was optogenetically inhibited. This finding was supported by measurement of increased cerebral blood flow in the deprived S1 after inhibition of its healthy counterpart as well as increased activation, as assessed with functional magnetic resonance imaging.

Li and colleagues suggest that with loss of peripheral input, the deprived S1 may be more susceptible to inhibitory signals of the healthy S1 traveling through the corpus callosum, the neuronal bridge across the hemispheres. This points to potential rehabilitation strategies that focus not simply on the injured nerve but on the healthy cortex. Although optogenetics can not yet “shed light” on the human brain, alternative techniques such as transcranial magnetic stimulation (which can also cause neuronal hyperpolarization) should be explored to help treat this potentially debilitating condition.

N. Li et al., Optogenetic-guided cortical plasticity after nerve injury. Proc. Natl. Acad. Sci. U.S.A. 108, 8838–8843 (2011). [Abstract]

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