Abstract
Norepinephrine modulates synaptic plasticity in various brain regions and is implicated in memory formation, consolidation and retrieval. The cerebellum is involved in motor learning, and adaptations of the vestibulo-ocular reflex (VOR) and optokinetic response (OKR) have been studied as models of cerebellum-dependent motor learning. Previous studies showed the involvement of adrenergic systems in the regulation of VOR, OKR and cerebellar synaptic functions. Here, we show differential contributions of β- and α2-adrenergic receptors in the mouse cerebellar flocculus to VOR and OKR control. Effects of application of β- or α2-adrenergic agonist or antagonist into the flocculus suggest that the β-adrenergic receptor activity maintains the VOR gain at high levels and contributes to adaptation of OKR, and that α2-adrenergic receptor counteracts the β-receptor activity in VOR and OKR control. We also examined effects of norepinephrine application, and the results suggest that norepinephrine regulates VOR and OKR through β-adrenergic receptor at low concentrations and through α2-receptor at high concentrations.
Highlights
The cerebellum is involved in motor learning, and adaptations of the vestibulo-ocular reflex (VOR) and optokinetic response (OKR) have been studied as models of motor learning[1,2,3,4]
Administration of isoproterenol into the left flocculus increased the OKR gain measured in the right eye from 0.33 ± 0.02 to 0.47 ± 0.02 (n = 6; p < 0.001, paired Student’s t-test), but did not affect the VOR gain (Fig. 1a–d) in accord with a previous report[13]
We showed that administration of β-adrenergic agonist into the flocculus increased the OKR gain but not the VOR gain, whereas administration there of β-adrenergic antagonist or α2-adrenergic agonist decreased the VOR gain and suppressed the gain-up adaptation of OKR
Summary
The cerebellum is involved in motor learning, and adaptations of the vestibulo-ocular reflex (VOR) and optokinetic response (OKR) have been studied as models of motor learning[1,2,3,4]. If the optokinetic stimulation continues for a certain time, the speed of the eyeball turn gets faster such that it can follow the screen movement better[3, 4] These phenomena are adaptations of VOR and OKR, which work to improve stabilization of the visual image on the retina during animal movement. It has been proposed that norepinephrine plays a role in modulation of cerebellum-dependent learning[18, 19], and injection of β-adrenergic antagonist into the rabbit flocculus diminishes the gain-up adaptation of VOR20, 21 It is not known whether the β-adrenergic receptor contributes to the gain increase adaptation of OKR induced by various training paradigms. We have addressed these questions and attempted to clarify the respective roles of β- and α2-adrenergic receptors in regulation and adaptations of VOR and OKR in mice
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