Noradrenergic influences on the cerebellar cortex: effects on vestibular reflexes under basic and adaptive conditions.
Experiments performed either in decerebrate cats or in intact rabbits have shown that functional inactivation of the cerebellar anterior vermis or the flocculus decreased the basic gain of the vestibulospinal or the vestibulo-ocular reflex, respectively. These findings were attributed to the fact that a proportion of the vermal or floccular Purkinje cells, which are inhibitory in function, discharge out of phase with respect to the vestibulospinal or the vestibulo-ocular neurons during sinusoidal animal rotation, thus exerting a facilitatory influence on the gain of the vestibular reflexes. Intravermal injection of a beta-noradrenergic agonist slightly increased the gain of the vestibulospinal reflex, whereas the opposite result was obtained after injection of beta-antagonists. Similarly, intrafloccular injection of a beta-noradrenergic agonist slightly facilitated the gain of the vestibulo-ocular reflex in darkness (but not in light), whereas a small decrease of the reflex occurred after injection of a beta-antagonist. It was postulated that the noradrenergic system acts on Purkinje cells by enhancing their amplitude of modulation to a given labyrinth signal, thus increasing the basic gain of the vestibular reflexes. The Purkinje cells of the cerebellar anterior vermis and the flocculus also exert a prominent role on the adaptation of vestibulospinal and vestibulo-ocular reflexes, respectively. In particular, intravermal or intrafloccular injection of beta-noradrenergic antagonists decreased or suppressed the adaptive capacity of the vestibulospinal and vestibulo-ocular reflexes that always occurred during sustained out-of-phase neck-vestibular or visual-vestibular stimulation, whereas the opposite result was obtained after local injection of a beta-noradrenergic agonist. The noradrenergic innervation of the cerebellar cortex originates from the locus coeruleus complex, whose neurons respond to vestibular, neck, and visual signals. It was postulated that this structure acts through beta-adrenoceptors to increase the expression of immediate-early genes, such as c-fos and Jun-B, in the Purkinje cells during vestibular adaptation. Induction of immediate-early genes could then represent a mechanism by which impulses elicited by sustained neck-vestibular or visuovestibular stimulation are transduced into long-term biochemical changes that are required for cerebellar long-term plasticity.
Dipartimento di Fisiologia e Biochimica, Università di Pisa, Italy.
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D000222:Adaptation, Physiological / Q000187:drug effects / Q000502:physiology*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D002415:Cats; D002525:Cerebellar Cortex / Q000187:drug effects / Q000502:physiology*; D003624:Darkness; D003655:Decerebrate State / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000502:physiology; D017781:Genes, Immediate-Early / Q000502:physiology; D008125:Locus Coeruleus / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology*; D011817:Rabbits; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D012027:Reflex, Vestibulo-Ocular / Q000187:drug effects / Q000502:physiology*
D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D009638:Norepinephrine