Membrane channel properties of premotor excitatory burst neurons may underlie saccade slowing after lesions of omnipause neurons.

Chemical lesions of the brain stem region containing glycinergic omnipause neurons (OPNs) cause saccade slowing with no change in latency. To explore the mechanisms responsible for this deficit, simulation studies were performed with a conductance-based model of premotor excitatory burst neurons (EBNs) that incorporated multiple membrane channels, including the T-type calcium channel. The peak speed of a normal saccade was determined by the T- and NMDA currents in EBNs after the OPNs shut off. After OPN lesions, the model made slow saccades, because the EBN activity was lower than normal due to a reduced T-current (caused by the loss of hyperpolarization), and a reduced NMDA current (caused by a reduced glycine concentration around the receptors). Thus, we propose that two biophysical mechanisms are responsible for saccade slowing after OPN lesions: reduced T-current and reduced NMDA current, both of which are caused by the loss of glycine from OPNs.