Uncrossed disynaptic inhibition of second-order vestibular neurons and its interaction with monosynaptic excitation from vestibular nerve afferent fibers in the frog. STRAKA, H. AND N. DIERINGER. Physiologisches Institut, Pettenkoferstr. 12, 80336 M[umlaut]unchen, Germany.
APStracts 3:0153N, 1996.
SUMMARY AND CONCLUSIONS
1. Eighth nerve evoked responses in central vestibular neurons (N=146) were studied in the isolated brainstem of frogs. 90% of these neurons responded with a monosynaptic EPSP following electrical stimulation of the ipsilateral VIIIth nerve. In 5% of these neurons the EPSP was truncated by a disynaptic IPSP and in 5% of these neurons a pure disynaptic IPSP was evoked. 2. Disynaptic IPSPs superimposed upon apparently pure EPSPs were revealed by bath application of the glycine receptor antagonist strychnine (0.5-5 [mu]M) or of the GABA A receptor antagonist bicuculline (0.5-2 [mu]M). The evoked EPSP increased in most central vestibular neurons (strychnine: 15 out of 16 neurons; bicuculline 26 out of 29 neurons). At higher stimulus intensities the evoked spike discharge increased from 2-3 spikes before to 8-10 spikes per electrical pulse during the application of blocking agents. The unmasked disynaptic inhibitory component increased with stimulus intensity to a different extent in different neurons. 3. Lesion studies demonstrated that these inhibitory components were generated ipsilaterally with respect to the recording side. The disynaptic strychnine sensitive inhibition was mediated by neurons located either in the ventral vestibular nuclear complex (VNC) or in the adjacent reticular formation. The spatial distribution of the disynaptic inhibition was investigated by simultaneous recordings of VIIIth nerve evoked field potentials at different rostro-caudal locations of the VNC. A significant strychnine sensitive component was detected in the middle and caudal part but not in the rostral part of the VNC. A bicuculline sensitive component was detected in the rostral and in the caudal part but not in the middle part of the VNC. In view of a similar rostro-caudal distribution of glycine- or GABA-immunoreactive neurons in the VNC of frogs our results suggest that part of the disynaptic inhibition is mediated by local interneurons with a spatially restricted projection area. 4. The monosynaptic EPSP of second-order vestibular neurons was mediated in part by N-methyl-D- aspartate (NMDA) and in part by non-NMDA receptors. The relative contribution of the NMDA receptor mediated component of the EPSP decreased with stronger stimuli. This negative correlation could have resulted from a preferential activation of NMDA receptors via thick vestibular nerve afferent fibers. Alternatively, the activation of NMDA receptors became disfacilitated at higher stimulus intensities due to the recruitment of disynaptic inhibitory inputs. Comparison of data obtained in the presence and in the absence of these glycine and GABA A receptor blockers indicates a preferential activation of NMDA receptors via larger diameter vestibular nerve afferent fibers. 5. The kinetics of NMDA receptors (delay, rise time) activated by afferent nerve inputs were relatively fast. These fast kinetics were independent of superimposed IPSPs. The association of these receptors with large diameter vestibular nerve afferent fibers suggests that fast NMDA receptor kinetics might be matched to the more phasic response dynamics of the large diameter vestibular afferent neurons to natural head accelerations.

Received 23 February 1996; accepted in final form 26 June 1996.
APS Manuscript Number J145-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996