Saccade Dysmetria in Head-Unrestrained Gaze Shifts After Muscimol Inactivation of the Caudal Fastigial Nucleus in the Monkey

Institut National de la Santé et de la Recherche Médicale /Université Claude Bernard-Lyon, Institut Fédératif des Neurosciences de Lyon, Bron.
Journal of Neurophysiology (Impact Factor: 2.89). 05/2005; 93(4):2343-9. DOI: 10.1152/jn.00705.2004
Source: PubMed


Lesions in the caudal fastigial nucleus (cFN) severely impair the accuracy of visually guided saccades in the head-restrained monkey. Is the saccade dysmetria a central perturbation in issuing commands for orienting gaze (eye in space) or is it a more peripheral impairment in generating oculomotor commands? This question was investigated in two head-unrestrained monkeys by analyzing the effect of inactivating one cFN on horizontal gaze shifts generated from a straight ahead fixation light-emitting diode (LED) toward a 40 degrees eccentric target LED. After muscimol injections, when viewing the fixation LED, the starting position of the head was changed (ipsilesional and upward deviations). Ipsilesional gaze shifts were associated with a 24% increase in the eye saccade amplitude and a 58% reduction in the amplitude of the head contribution. Contralesional gaze shifts were associated with a decrease in the amplitude of both eye and head components (40 and 37% reduction, respectively). No correlation between the changes in the eye amplitude and in head contribution was observed. The amplitude of the complete head movement was decreased for ipsilesional movements (57% reduction) and unaffected for contralesional movements. For both ipsilesional and contralesional gaze shifts, the changes in eye saccade amplitude were strongly correlated with the changes in gaze amplitude and largely accounted for the gaze dysmetria. These results indicate a major role of cFN in the generation of appropriate saccadic oculomotor commands during head-unrestrained gaze shifts.

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    • "Unilateral FOR inactivation also impairs the ability to fixate small targets: when compared with the positions taken before inactivation, the gaze is directed toward positions that are shifted by ϳ1° toward the side of the injection, whether the head is restrained (Goffart et al. 2004; Robinson et al. 1993) or unrestrained (Quinet and Goffart 2005). The shifted spatial distribution of dwell times in Fig. 2B illustrates this change in gaze orientation, a disorder that has been called " fixation offset. "
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    • "Independent control of the eyes and head occurs naturally at the level of the extraocular and neck motoneurons, although some form of separate processing has also been proposed to occur in cortical (Chen 2006; Chen and Walton 2005; Constantin et al. 2004, 2006), subcortical (Gandhi and Walton 2006; Pathmanathan et al. 2005a,b; Walton and Gandhi 2006), and cerebellar (Quinet and Goffart 2005) structures. It has been hypothesized that head movements associated with gaze shifts are driven by at least two parallel pathways: one is gated by the pontine omnipause neurons (OPNs) and issues movement commands to the eyes and head and the other bypasses the OPN gate and does not encode a saccadic eyemovement command (Corneil et al. 2002; Galiana and Guitton 1992; Goossens and Van Opstal 1997; Guitton et al. 1990). "
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