Abstract

Compensatory head movements as responses to passive angular acceleration are obvious in lower vertebrates, but they are usually small and difficult to observe in mammals. The may simply be cut short very early by an inhibitory mechanism linked to the initiation of anticompensatory head movements (quick phases of head nystagmus). After electrolytic lesions of the pontine reticular formation (PRF), rats made no spontaneous lateral head movements, but exhibited large compensatory lateral head movements and abnormal postrotatory circus movements, both of which can be regarded as consequences of a loss of the quick phase of head nystagmus. The quick phase of ocular nystagmus was also lost, corroborating earlier findings of others in primates, cats, and rabbits, and supporting the view that saccadic movements of the head and eyes are generated by closely related neural substrates. Rats with bilateral PRF lesions were unable to right themselves in the air. Together with additional observations, this indicates involvement of the PRF in some functions of the otolith organ.

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