Nystagmus induced by pharmacological inactivation of the brainstem ocular motor integrator in monkey

被引:54
作者
Arnold, DB
Robinson, DA
Leigh, RJ
机构
[1] Univ Hosp Cleveland, Dept Neurol, Cleveland, OH 44106 USA
[2] Univ Hosp Cleveland, Dept Neurosci, Cleveland, OH 44106 USA
[3] Univ Hosp Cleveland, Dept Biomed Engn, Cleveland, OH 44106 USA
[4] Johns Hopkins Sch Med, Dept Ophthalmol & Biomed Engn, Baltimore, MD USA
[5] Case Western Reserve Univ, Vet Affairs Med Ctr, Cleveland, OH 44106 USA
关键词
nystagmus; GABA; NMDA; cerebellum; neural integrator;
D O I
10.1016/S0042-6989(99)00142-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A common cause of pathological nystagmus is malfunction of the mechanism by which the brain integrates eye velocity signals to produce eye position commands. For horizontal gaze, neurons in the nucleus prepositus hypoglossi-medial vestibular nucleus region (NPH-MVN) play a vital role in this neural integrator function. We studied the effects on gaze stability of pharmacological intervention in the NPH-MVN of monkeys by microinjections of eight drugs. Agents with agonist or antagonist actions at gamma-aminobutyric acid (GABA), glutamate, and kainate receptors all caused gaze-evoked nystagmus with centripetal eye drifts; glycine and strychnine had no effect. When the GABA(A)-agonist muscimol was injected near the center of MVN, the eyes drifted away from the central position with increasing-velocity waveforms, implying an unstable neural integrator. The observed effects of these drugs on gaze stability may be related to inactivation either of neurons within NPH-MVN or the cerebellar projections to them that control the fidelity of neural integration. Drugs that influence GABA or glutamine transmission may have a role in the treatment of nystagmus due to an abnormal neural integrator. Published by Elsevier Science Ltd.
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页码:4286 / 4295
页数:10
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