Abstract
Pontine short-lead burst neurons (SLBNs) carry the final output signal of the horizontal saccade generator. Our previous study has shown that these SLBNs receive glycinergic inhibitory input during contraversive (off-direction) saccades and that this inhibition does not originate from omnipause neurons (OPNs). In the present study, we examined a possible contribution of inhibitory input to the formation of burst activity of SLBNs for ipsiversive (on-direction) saccades, activity that determines the size and velocity of movements. Using three-barrelled micropipettes, we recorded extracellular spike activity of SLBNs and applied iontophoretically a glycine receptor antagonist, strychnine, in the alert cat. Off-line analysis calculated parameters of neuronal activity and of eye movements. Inspection of the relation between the mean burst firing rate and the mean horizontal velocity of saccades revealed an increase in burst activity after drug application. We tested statistically whether the regression lines of this relation for pre- and postapplication data were different. No significant difference was found in the slope of the regression line, but the y-intercept was significantly larger after application in the majority of neurons. Results indicate that, during on-direction saccades, SLBNs receive an inhibitory input of non-OPN origin that significantly reduces the effect of a concomitant excitatory drive, thereby shaping the final saccadic signal. [Jpn J Physiol 54 Suppl:S180 (2004)]
