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While mice deficient in EAAT1, which is highly expressed in cerebellar astrocytes, did not show changes in cerebellar structure or obvious symptoms of cerebellar impairment such as ataxic gait, they were unable to adapt to more challenging motor tasks such as quickly running on the rotorod (Watase et al., 1998)

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Considerable efforts have been dedicated to unraveling the role of cation (sodium, potassium and calcium) channels in the pathogenesis of CIPN (Price et al., 2009)

Double-blind clinical trials evaluating endurance athletes have shown that supplementing with this combination significantly reduces the incidence of upper respiratory tract infections post-exertion and accelerates the clearance of inflammatory proteins associated with delayed onset muscle soreness