Direct inhibitory projection of pause neurons to nystagmus-related pontomedullary reticular burst neurons in the cat.

Abstract

Brainstem pause neurons (PNs) exhibit a tonic discharge during the slow phase of horizontal vestibular nystagmus and pause prior to and during the quick phase in both directions. One type of pontomedullary burst neurons, burst inhibitory neurons (BINs), show a high frequency burst of spikes before and during the quick phase to the ipsilateral side and this burst directly inhibits contralateral abducens motoneurons, terminating the slow phase firing of these motoneurons. The present study focused on synaptic relations between PNs and BINs. The following data supported the conclusion that PNs probably make direct inhibitory connections with BINs and produce IPSPs in BINs during the slow phase of horizontal vestibular nystagmus: (a) there were positive field potentials in the BIN area during the slow phase; (b) PNs were antidromically activated from BIN areas bilaterally; (c) systematic microstimulation of the BIN area revealed a pattern consistent with axonal branching in the BIN area; (d) repetitive microstimulation of the PN area induced a positive shift in the field potential in the BIN area and suppressed both the characteristic bursts of BINs and nystagmic activity of the contralateral abducens nerve; (e) microstimulation of the PN area during intracellular recording of BINs induced monosynaptic latency hyperpolarizing potentials which could be reversed by C1- injection; (f) during intracellular recording from BINs during vestibular nystagmus in either direction, the membrane potential during the slow phases had a tonic hyperpolarization which was shown to be due to IPSPs by means of C1- injection. This study suggests that burst activity of BINs during the quick phase is caused by abrupt release from PN IPSPs (disinhibition), besides some excitatory inputs from other sources.