Ketamine induces failure of the oculomotor neural integrator in the cat
References (18)
- et al.
Intracellular demonstration of an receptor mediated component of synaptic transmission in the rat hippocampus
Neurosci. Lett.
(1985) - et al.
Implantation of magnetic search coils for measurement of eye position: an improved method
Vision Res.
(1980) - et al.
Ketamine acts as a non-competitive antagonist on frog spinal cord in vitro
Neuropharmacology
(1985) The effect of cerebellectomy on the cat's vestibuloocular integrator
Brain Res.
(1974)- et al.
Selective blockade of an excitatory synapse in rat cerebral cortex by the sigma opiate cyclazocin: an intracellular in vitro study
Neurosci. Lett.
(1985) - et al.
The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N-methyl-aspartate
Br. J. Pharmacol.
(1983) - et al.
Loss of the neural integrator of the oculomotor system from brain stem lesions in monkey
J. Neurophysiol.
(1987) - et al.
Disabling of the oculomotor neural integrator by kainic acid injections in the prepositus-vestibular complex of the cat
J. Physiol.
(1987) - et al.
Lesions in the cat prepositus complex: effects on the vestibulo-ocular reflex and saccades
J. Physiol.
(1986)
Cited by (33)
Pharmacological treatment effects on eye movement control
2008, Brain and CognitionKetamine-induced distractibility: An oculomotor study in monkeys
2005, Biological PsychiatryCitation Excerpt :At the end of the saccade, the maintenance of the eyes in an eccentric position, i.e., against the elastic restoring forces that would otherwise pull back the eyes toward a central position, depends on an eye position signal that is obtained by neural integration of the saccadic pulse. A gaze-evoked nystagmus, such as observed in our monkeys after ketamine injection, results from the impairment of this neuronal integration normally performed in the nucleus prepositus hypoglossi (Godaux et al 1990; Mettens et al 1990). The presence of this nystagmus, evident within a few minutes after ketamine injection (Figure 5), renders a double-blind study unrealizable.
Frequency-dependent effects of glutamate antagonists on the vestibulo-ocular reflex of the cat
2000, Brain ResearchCitation Excerpt :Like APV and MK-801, ketamine caused a transient ataxia, a reduction in the number of spontaneous saccades, and an exponential drift toward the center of gaze following each saccade. Others have described the post-saccadic drift in more detail [24]. NBQX, a potent antagonist at both AMPA and kainate receptors but not at NMDA receptors, selectively attenuated the high-frequency VOR.
Does ketamine-mediated N-methyl-D-aspartate receptor antagonism cause schizophrenia-like oculomotor abnormalities?
1998, NeuropsychopharmacologyThe contribution of N-methyl-D-aspartate receptors to lesion-induced plasticity in the vestibular nucleus
1997, Progress in Neurobiology