Effects of nucleus prepositus hypoglossi lesions on visual climbing fiber activity in the rabbit flocculus

The caudal dorsal cap (dc) of the inferior olive is involved in the control of horizontal compensatory eye movements. It provides those climbing fiber s to the vestibulocerebellum that modulate optimally to optokinetic stimula tion about the vertical axis. This modulation is mediated at least in part via an excitatory input to the caudal dc from the pretectal nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system. In addition, the caudal dc receives a substantial GABAergic input from the nucleus prepositus hypoglossi (NPH). To investigate the possible contributi on of this bilateral inhibitory projection to the visual responsiveness of caudal dc neurons, we recorded the climbing fiber activity (i.e., complex s pikes) of vertical axis Purkinje cells in the flocculus of anesthetized rab bits before and after ablative lesions of the NPH. When the NPH ipsilateral to the recorded flocculus was lesioned, the spontaneous complex spike firi ng frequency did not change significantly; but when both NPHs were lesioned , the spontaneous complex spike firing frequency increased significantly. W hen only the contralateral NPH was lesioned, the spontaneous complex spike firing frequency decreased significantly. Neither unilateral nor bilateral lesions had a significant influence on the depth of complex spike modulatio n during constant velocity optokinetic stimulation or on the transient cont inuation of complex spike modulation that occurred when the constant veloci ty optokinetic stimulation stopped. The effects of the lesions on the spont aneous complex spike firing frequency could not be explained when only the projections from the NPH to the inferior olive were considered. Therefore w e investigated at the electron microscopic level the nature of the commissu ral connection between the two NPHs. The terminals of this projection were found to be predominantly GABAergic and to terminate in part on GABAergic n eurons. When this inhibitory commissural connection is taken into considera tion, then the effects of NPH lesions on the spontaneous firing frequency o f floccular complex spikes are qualitatively explicable in terms of relativ e weighting of the commissural and caudal dc projections of the NPH. In sum mary, we conclude that in the anesthetized rabbit the inhibitory projection of the NPH to the caudal dc influences the spontaneous firing frequency of floccular complex spikes but not their modulation by optokinetic stimulati on.