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could be treated with Microarray LEDs [12] while deeper areas would have
some delivery system consisting of fiber optic wires [22]. Finally any issues of
plasticity, whether Hebbian or homeostatic [9] [10] must be addressed when
repeatedly activating an ectopic cation channel and the consequent implication
on rehabilitation.
4 Discussion and Conclusions
Problems associated with conventional electrical stimulation of neurons include:
-
Electrical stimuli can excite action potentials but cannot inhibit neuron ac-
tivity.
-
It is dicult to confine electrical fields to target specific cell types or struc-
tures.
-
Possible alterations in neural tissue due to power dissipation (specially for
large arrays of stimulators).
Here we propose to use light activated channels as alternative approach for
chronic stimulations, which could resolve some of these issues. In this context
examples of optogenetic control of movement in rodents using fiber optic wires
and ChR2 expression in the motor cortex have already been succesfully demon-
strated [20]. Advances in the field of optogenetics have engineered new ChR2
versions making it possible to achieve sustained spike trains up to at least 200Hz
[27]. In addition ChR2 has been mutated into a step-function opsin (SFO) mak-
ing neurons in a state of increased exciteability after brief pulses of light which
can then in turn be reversed by a pulse of yellow light [28].
However, it still remains to be seen if these tool and its advances can restore
biologically relevant activity to effected brain areas as it has mostly been used
as an exploratory tool. Recently the potential of this tool in rehabilitation was
explored experimentally in muscle control. In movement rehabilitiation stimu-
lation with electric cuffs so far has been disappointing. The reason for this is
because it tends to recruit large, fatigable motor neurons and not the smaller
motor neurons. The significance of this to paralyzed patients is that although
they are able to walk when electrically stimulated, this is only sustainable for
several minutes as larger fast twitch nerve fibers respond preferentially to the
small-slow twitch nerves. As it is the smaller nerve fibers that contol refined
movement their absence during activation results in jerky movement and rapid
fatigue. Promisingly, optogenetic stimulation of mouse peripheral nerves seems
to achieve the orderly recruitment of these muscles enhancing perfomance while
concurrently reducing fatigue [29]. Should these experiments prove fruitfull the
use of alternative light sensitive proteins which inhibit activity could help allevi-
ate diseases in which hyperexciteability causes spasticity such as in cerebral pulsy
or convulsion in epilepsy. Such a tool already exists in the form of the chloride
pump, Halorhodopsin which is activated by yellow light [30]. The addition of
this protein to the optogentic tool box now also permits for controlled inhibition
of neural activity. This will be necessary when considering gabaergic inhibitory
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