1. Unit spikes of burst neurons were extracellularly recorded in the pontomedullary reticular formation of the cat. These neurons were identified by their burst activity coincident with the quick inhibitory phase of the contralateral abducens nerve during vestibular nystagmus and their antidromic activation from the contralateral abducens nucleus. 2. When the extracellular field potentials in and near the abducens nucleus were triggered by spikes of a contralateral burs neuron, the averaged potential consisted of an early di- or triphasic spike and a late slow positive wave. The early spike was an action current caused by impulses conducting along the axon of the burst neuron. 3. The action potentials of a contralateral burst neuron. 3. The action potentials of a contralateral burst neuron were employed to trigger a post-spike average of the membrane potential of abducens motoneurons. Then unitary IPSPs with monosynaptic latencies were revealed. This provided direct evidence that the burst neurons are inhibitory in nature. The amplitudes of unitary IPSPs ranged from 18 to 220 mu V. Each inhibitory burst neuron branched widely in the abducens nucleus and was estimated to make inhibitory connections with approximately 60% of the motoneuron pool. 4. The post-spike average of compound potentials of the abducens nerve triggered by action potentials of contralateral single inhibitory burst neurons revealed inhibition of spike activity with latencies and time courses compatible with those of unitary IPSPs in motoneurons. The inhibition was observed with all inhibitory burst neurons tested.

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.

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The axonal projections of 62 posterior canal (PC)-activated excitatory and inhibitory secondary vestibular neurons were studied electrophysiologically in cats. PC-related neurons were identified by monosynaptic activation elicited by electrical stimulation of the vestibular nerve and activation following nose-up rotation of the animal's head. Single excitatory and inhibitory neurons were identified by antidromic activation following electrical stimulation of the contralateral and ipsilateral medial longitudinal fasciculus, respectively. The oculomotor projections of identified neurons were confirmed with a spike-triggered averaging technique. The axonal projections of the identified neurons were then studied by systematic, antidromic stimulation of the mesodiencephalon. Excitatory neurons showed two main types of axonal projections. In one type, axonal branches were issued to the interstitial nucleus of Cajal, central gray, and thalamus including the ventral posterolateral, ventral posteromedial, ventral lateral, ventral medial, centromedian, central lateral, lateral posterior, and ventral lateral geniculate nuclei. The other type was more frequently observed, giving off axon collaterals to the above-mentioned regions and to Forel's field H as well. Inhibitory neurons issued axonal branches to limited areas which included the central gray, interstitial nucleus of Cajal, its adjacent reticular formation and caudalmost part of Forel's field H, but not the rostral part of the Forel's field H and the thalamus. These results suggest that PC-related excitatory neurons participate in the genesis of vertical eye movements and in the perception of the vestibular sensation, and that PC-related inhibitory neurons seem to take part only in the genesis of vertical eye movements.

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