1. For horizontal eye movements, previous observations led to the hypothesis that the legendary neural integrator necessary for correct gaze holding, adequate vestibuloocular reflex (VOR), and optokinetic nystagmus, was located in the region of the complex formed by the nucleus prepositus hypoglossi (NPH) and the medial vestibular nucleus (MVN). 2. The aim of the present study was to test the respective contributions of the NPH, of the rostral part of the MVN, which contains most second-order vestibular neurons, and of the central part of the MVN to the horizontal integrator. 3. An injection of muscimol was used to inactivate each of these three zones in the cat's brain. Muscimol is a gamma-aminobutyric acid (GABA) agonist. By binding to GABAA receptors, it induces a hyperpolarization of the neurons that nullifies their activity. Muscimol was injected into the brain stem of the alert cat through a micropipette by an air pressure system. 4. The search coil technique was used to record spontaneous eye movements and the VOR induced by rotating a turntable at a constant velocity. VOR was analyzed by a new method: transient analysis of vestibular nystagmus. 5. A unilateral injection of muscimol into the NPH induced a bilateral gaze-holding failure: saccades were followed by a centripetal postsaccadic drift. A vestibular imbalance was also present but it was moderate and variable. The VOR responses were distorted drastically. Through transient analysis of vestibular nystagmus, that distortion was revealed to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator. The responses to a rotation either toward the injected side or in the opposite direction were asymmetrical. The direction of that asymmetry was variable. 6. A unilateral injection of muscimol into the rostral part of the MVN caused a vestibular imbalance: in complete darkness, a nystagmus appeared, whose linear slow phases were directed toward the side of injection. 7. A unilateral injection of muscimol into the central part of the MVN induced a syndrome where a severe bilateral gaze-holding failure was combined with a vestibular imbalance. In the light, saccades were followed by a bilateral centripetal postsaccadic drift. In complete darkness, a nystagmus was observed, whose curved slow phases were directed towards the side of injection. The VOR responses were distorted drastically. Here again, that distortion was revealed by our analysis to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator.(ABSTRACT TRUNCATED AT 400 WORDS)

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SUMMARY1. In order adequately to control eye movements, oculomotoneurones have to be supplied with both an eye-velocity signal and an eye-position signal. However, all the command signals of the oculomotor system are velocity signals. Nowadays, there is general agreement about the existence of a brainstem network that would convert velocity command-signals into an eye-position signal. This circuit, because of its function, is called the oculomotor neural integrator. The most obvious symptom of its eventual failure is a gaze-holding deficit: in this case, saccades are followed by a centripetal post-saccadic drift. Although the oculomotor neural integrator is central in oculomotor theory, its precise location is still a matter for debate.2. Previously, microinjections of kainic acid (KA) into the region of the nucleus prepositus hypoglossi (NPH) and of the medial vestibular nucleus (MVN) were found to induce a horizontal gaze-holding failure both in the cat and in the monkey.However, the relatively large volumes (1-3 pl) and concentrations (2-4 ,ug j#ll) used in these injections made it difficult to know if the observed deficit was due to a disturbance of the NPH or of the nearby MVN. These considerations led us to inject very small amounts of kainic acid (50 nl, 0.1 jtg jtl-) either into the rostral part of the MVN or into different sites along the NPH of the cat.3. The search coil technique was used to record (1) spontaneous eye movements (2) the vestibulo-ocular reflex (VOR) induced by a constant-velocity rotation (50 deg s-1 for 40 s) and the optokinetic nystagmus (OKN) elicited by rotating an optokinetic drum at 30 deg s-1 for 40 s.4. In each injection experiment, the location of the abducens nucleus of the alert cat was mapped out by recording the antidromic field potentials evoked by the stimulation of the abducens nerve. Two micropipettes were then glued together in such a way that when the tip of the recording micropipette was in the centre of the abducens nucleus the tip of the injection micropipette was in a target area. The twin pipettes were then lowered in the brainstem until the recording micropipette reached the centre of the abducens nucleus. Kainic acid was then injected into the brainstem of the alert cat through the injection micropipette by an air pressure system. 5. Carried out according to such a protocol, KA injections into the NPH or the rostral part of the MVN consistently led to specific eye-movement changes. A unilateral injection into the NPH caused a bilateral horizontal gaze-holding failure MS 2099 E. GODAUX, P. METTENS AND G. CHERON without any spontaneous nystagmus or any significant deviation of the null-position of the gaze. A unilateral injection into the rostral MVN, for its part, induced a nystagmus whose slow phases were linear and directed to the contralateral side. No gaze-holding deficit accompanied this vestibular imbalance.6. Taken together with the data from the literature showing that the principal signal carried by the neurones of the NPH is an eye-position signal,...

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