A review of age-related changes in cerebellar β-adrenergic function and associated motor learning

The present review provides an overview of age-related changes in cerebellar β-adrenergic function, associated motor learning, causal agents and possible treatments. Norepinephrine acts as a neuromodulator of Purkinje cell activity. With aging, however, the ability of norepinephrine to modulate Purkinje cell activity and specifically GABAergic inhibition of Purkinje cell activity is decreased. This age-associated deficit in cerebellar noradrenergic function correlates with deficits in acquisition of a motor learning task. Aged rats are delayed in acquiring a motor learning task that requires rats to adjust footfalls in order to cross a runway. The degree of deficit in cerebellar β-adrenergic activity correlated positively with the degree of impairment in task acquisition. One possible causal agent for the β-adrenergic deficit is free radical damage. Hyperoxia, which may generate free radical damage, induces cerebellar β-adrenergic deficits in young rats but diet restriction and treatment with antioxidants can delay or reverse age-related deficits in cerebellar β-adrenergic function in old rats.