Gould T J
Age (Omaha). 1999 Jan;22(1):19-25. doi: 10.1007/s11357-999-0003-6.
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.
本综述概述了小脑β-肾上腺素能功能、相关运动学习、致病因素和可能的治疗方法的年龄相关变化。去甲肾上腺素作为浦肯野细胞活动的神经调质。然而，随着年龄的增长，去甲肾上腺素调节浦肯野细胞活动的能力，特别是对浦肯野细胞活动的GABA能抑制作用会降低。小脑去甲肾上腺素能功能的这种与年龄相关的缺陷与运动学习任务获取方面的缺陷相关。老年大鼠在获取一项要求大鼠调整脚步以穿过跑道的运动学习任务时会延迟。小脑β-肾上腺素能活性的缺陷程度与任务获取的受损程度呈正相关。β-肾上腺素能缺陷的一个可能致病因素是自由基损伤。可能产生自由基损伤的高氧会在幼鼠中诱发小脑β-肾上腺素能缺陷，但饮食限制和抗氧化剂治疗可以延缓或逆转老年大鼠小脑β-肾上腺素能功能的年龄相关缺陷。
