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Daily addition of acetyl-L-carnitine (100 microM) to cultured cerebellar granule cells since the first day of maturation led to an increased rate of expression of D-[3H]aspartate uptake (an established marker of maturation of glutamatergic neurons) and of N-methyl-D-aspartate (NMDA) receptors linked to large conductance ion channels permeable to Ca2+. Acetyl-L-carnitine treatment also increased neuronal survival, as reflected by a greater percentage of cultures retaining functional NMDA receptors after 15 days of maturation. These results support the view that acetyl-L-carnitine exerts neuronotrophic activity and prevents age-dependent neuronal degeneration.

NMDA-sensitive glutamate receptors are involved in the regulation of neuronal plasticity, and contribute to the synaptic mechanisms underlying the learning process. Aging is associated with a reduction in the maximal density of NMDA-sensitive glutamate binding sites in rat hippocampus. This reduction is attenuated after long-term administration with L-acetylcarnitine (10 mg/Kg i.p. once a day for 4 months). These results support a neuroprotective and neurotrophic role for L-acetylcarnitine during aging.