Role of Glycinergic Inhibition in Shaping Activity of Saccadic Burst Neurons

Abstract

The immediate premotor signals for saccades are created at the level of medium-lead burst neurons (MLBNs). During fixations, MLBNs receive tonic inhibition from omnipause neurons (OPNs), which use glycine as a neurotransmitter. To elucidate the role of this inhibition, we studied discharge patterns of horizontal MLBNs following iontophoretic application of strychnine, a glycine-receptor antagonist, in alert cats. Three-barrel micropipettes were used for extracellular recording and iontophoresis. After application of strychnine, MLBNs exhibited spontaneous discharge and visual responses during intersaccadic intervals. Spikes were evoked by single-pulse stimulation of the contralateral superior colliculus (SC). These results show that MLBNs receive substantial excitatory input during intersaccadic intervals and that inhibitory action of OPNs is indeed necessary to prevent MLBNs from firing. Strychnine also affected saccade-related activity of MLBNs. The burst of activity, as in normal conditions, declined rapidly before the end of saccades but was followed by low rate spike activity, which continued beyond the end of saccades. This suggests that in normal conditions, the termination of saccades is determined by resumed inhibitory action of OPNs and not by termination of excitatory input to MLBNs. In addition, the firing rate and the number of spikes during saccades increased after strychnine application, suggesting that MLBNs receive glycinergic inhibition of non-OPN origin as well. We conclude that glycinergic inhibition plays essential roles in the maintenance of stable fixation, the termination of saccades, and the regulation of saccade size and velocity.