Российская академия наук


MECHANISMS OF NEUROPROTECTION AND NEUROPLASTICITY AFTER REPETITIVE TRANSORBITAL ALTERNATING CURRENT STIMULATION



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MECHANISMS OF NEUROPROTECTION AND NEUROPLASTICITY AFTER REPETITIVE TRANSORBITAL ALTERNATING CURRENT STIMULATION

Sergeeva E.G.

Institute of Medical Psychology, University of Magdeburg, Germany, elena.sergeeva@med.ovgu.de


Current stimulation is emerging as a new tool to manipulate central nervous system plasticity and restoration. Most recently, we have induced recovery of vision by applying non-invasive repetitive transorbital alternating current stimulation to patients with optic nerve damage. It was proposed that visual field improvements were mediated by increased neuronal synchronization of residual visual system structures and higher cortical areas.

For a better understanding of the mechanisms of action of current stimulation experiments in animals are required. In preclinical studies using animal models it was revealed that transcorneal alternating current stimulation (tACS) decreases acute death of retinal ganglion cells (RGCs) after optic nerve transection in rats, but it is not known if cell survival is long-term and associated with functional restoration. We therefore evaluated the effects of tACS in a rat model of optic nerve crush (ONC) based on anatomical, electrophysiological and behavioural measures to clarify the potential domain(s) where the stimulation has an effect and to further understand possible prerequisites of functional restoration.

Our results suggest that tACS induced long-term neuronal protection specifically from delayed retrograde cell death after severe axonal damage but did not improve visual performance in a behavioural test. Also it was not

associated with changes in bioelectrical activity (EEG, VEP – visual evoked potentials), recorded from visual cortex. However, we demonstrated that tACS can induce neuroplasticity in rodents under certain circumstances, as shown by EEG “after-effects” that outlast the stimulation period. But this “after-effects” are not seen when tACS is applied during deep anaesthesia and not when applied to animals after severe optic nerve damage. We conclude that tACS requires a minimal level of brain activation and is only effective to induce cortical plasticity when the retina can be excited.

To avoid this problem of low functional state of brain under narcosis, we set up a new preclinical tACS model with unanaesthetized, freely-moving rats. The animals are stimulated via fine wire electrodes implanted under the upper eyelid, and field potentials are recorded from visual cortex and superior colliculus.

This technique enables us to find electrophysiological correlates of tACS and report for the first time electrically evoked responses (EERs) by tACS in visual cortex of freely-moving animals. Evaluation of amplitudes and latencies of components can reveal the EER origin, particularly when comparing the EER with VEP. Thereby, it will be possible to identify the target site for tACS treatment and clarify optimal parameter settings for tACS to achieve maximal visual responses.

With our experiments in rodents we like to further understand tACS and based on this to optimise the treatment. Our results suggest that tACS acts via different mechanisms (neuroprotection as well as neuroplasticity) and on different target structures (from retina to visual cortex).


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