2517048

[Eye movement is controlled by basal ganglia-induced GABAergic inhibition].

Article date: 1989/12/1

PubMed ID: 2517048

Journal name: Rinsho shinkeigaku = Clinical neurology (ISSN: 0009-918X)

ABSTRACT

Saccadic eye movement is controlled by a midbrain structure, superior colliculus (SC). Cells in its intermediate layer show a burst of spikes before saccades to the contralateral disc. A major input to the SC comes from the substantia nigra pars reticulata (SNr). SNr cells are characterized by their high frequency tonic discharge. Many of them stop discharging before a contralateral saccade only when the saccade is made intentionally. The mirror image-like relationship between the SNr and the SC suggests that the nigro-collicular connection is inhibitory. To determine whether the nigro-collicular inhibition is necessary for normal eye movements, we injected a small amount of GABA-related substances into the SC or the SNr. Following injection of muscimol (GABA agonist) into the SC, contralateral saccades became delayed, hypometric and slower; the monkey finally became unable to make saccades. This result indicated that the SC is crucial for normal saccades and that SC cells have ample GABA receptors. Following injection of bicuculline (GABA antagonist), irrepressible saccades occurred repeatedly to the contralateral side, suggesting that SC cells are under tonic inhibition which is mediated by GABA. Similar involuntary saccades were induced by injection of muscimol into the SNr. This suggested that the SNr is the origin of the GABAergic tonic inhibition. These results suggested that the basal ganglia control the initiation of saccadic eye movement by changing the level of the nigro-collicular inhibition.

Author List: Hikosaka O

Publication Types: English Abstract; Journal Article; Review

Substances mentioned in the article: gamma-Aminobutyric Acid;

Mesh terms: Animals; Basal Ganglia/physiology; Eye Movements; Haplorhini; Neural Inhibition; Saccades; Substantia Nigra/physiology; Superior Colliculi/physiology; gamma-Aminobutyric Acid/physiology;

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