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Noradrenergic agents in the cerebellar vermis affect adaptation of the vestibulospinal reflex gain.

作者信息

Pompeiano O, Manzoni D, D'Ascanio P, Andre P

机构信息

Dipartimento di Fisiologia e Biochimica, Università di Pisa, Italy.

出版信息

Brain Res Bull. 1994;35(5-6):433-44. doi: 10.1016/0361-9230(94)90156-2.

Abstract

In precollicular decerebrate cats, the vestibulospinal reflex (VSR) was intermittently recorded from the triceps brachii during sinusoidal roll tilt of the whole animal (at 0.15 Hz, +/- 10 degrees), leading to selective stimulation of labyrinth receptors. This reflex, tested during and after a 3-h period of sustained animal tilt at the same parameters indicated above, showed an adaptive increase in gain in some experiments but not in others. In a second group of experiments, however, rotation of the head (at 0.15 Hz, +/- 10 degrees) was associated with a synchronous body rotation (at 0.15 Hz, +/- 12.5 degrees) which led to an additional neck input, due to 2.5 degrees of out-phase body-to-head displacement. In these experiments, the VSR, tested every 10-15 min, consistently showed an adaptive increase in gain during and after a 3-h period of sustained vestibular and neck stimulation. Microinjection into the cerebellar anterior vermis of beta-adrenergic agents (0.25 microliters at 8 micrograms/microliters saline) produced slight and short-lasting changes in the basic amplitude of the VSR, due to the neuromodulatory influence of these agents on the Purkinje cells activity. In addition, the beta-adrenergic agonist isoproterenol brought to the light an adaptive process in those experiments in which no adaptation occurred during a sustained roll tilt of the whole animal. On the other hand, the beta-adrenergic antagonists propranolol or sotalol either suppressed the increase in gain of the VSR which occurred in other experiments during sustained animal rotation, or prevented the occurrence of an adaptive increase in gain during a continuous out-phase head and body rotation. We conclude that the adaptive changes in gain of the VSR are facilitated by the noradrenergic system acting within the cerebellar cortex through beta-adrenoceptors.

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