Abstract
Beyond the optimal frequency range of excitation, central nystagmus is not sustained, but dies out during stimulation. Small doses of chlorpromazine (250 μg/kg) shift the optimum to higher frequencies and prolong the after-nystagmus. Large doses of the drug diminish the intensity of the nystagmus response. This differential action of chlorpromazine is interpreted as a selective effect of small doses on the inhibitory components of the nystagmus circuit, which are distinguished from the excitatory elements by their electrophysiological properties.
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