Contributions of regularly and irregularly discharging vestibular-nerve inputs to the discharge of central vestibular neurons in the alert squirrel monkey

1997 ◽  
Vol 114 (3) ◽  
pp. 405-422 ◽  
Author(s):  
C. Chen-Huang ◽  
Robert A. McCrea ◽  
Jay M. Goldberg
Keyword(s):  
Squirrel Monkey ◽  
Vestibular Nerve ◽  
Vestibular Neurons

Projection of the vestibular nerve to the area 3a arm field in the squirrel monkey (Saimiri Sciureus)

1974 ◽  
Vol 21 (1) ◽  
Author(s):  
L.M. �dkvist ◽  
D.W.F. Schwarz ◽  
J.M. Fredrickson ◽  
R. Hassler
Keyword(s):  
Squirrel Monkey ◽  
Vestibular Nerve ◽  
Saimiri Sciureus ◽  
Area 3A

Morphometry and Ultrastructure of the Squirrel Monkey (Saimii sciureus)Vestibular Nerve

1987 ◽  
Vol 129 (3) ◽  
pp. 188-199 ◽  
Author(s):  
Cesar D. Fermin ◽  
Makoto Igarashi
Keyword(s):  
Squirrel Monkey ◽  
Vestibular Nerve

Uncrossed disynaptic inhibition of second-order vestibular neurons and its interaction with monosynaptic excitation from vestibular nerve afferent fibers in the frog

1996 ◽  
Vol 76 (5) ◽  
pp. 3087-3101 ◽  
Author(s):  
H. Straka ◽  
N. Dieringer
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Large Diameter ◽  
Vestibular Nerve ◽  
Vestibular Neurons ◽  
Postsynaptic Potential ◽  
Afferent Fibers ◽  
Viiith Nerve ◽  
Disynaptic Inhibition ◽  
Preferential Activation

1. Eighth nerve evoked responses in central vestibular neurons (n = 146) were studied in the isolated brain stem of frogs. Ninety percent of these neurons responded with a monosynaptic excitatory postsynaptic potential (EPSP) after electrical stimulation of the ipsilateral VIIIth nerve. In 5% of these neurons, the EPSP was truncated by a disynaptic inhibitory postsynaptic potential (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 microM) or of the gamma-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (0.5–2 microM). 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 to 3 spikes before up 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 rostrocaudal locations of the VNC. A significant strychnine-sensitive component was detected in the middle and caudal parts but not in the rostral part of the VNC. A bicuculline-sensitive component was detected in the rostral and in the caudal parts but not in the middle part of the VNC. In view of a similar rostrocaudal distribution of glycineor 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 GABAA 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.

Neuronal activity in the ipsilateral vestibular nucleus following unilateral labyrinthectomy in the alert guinea pig

1995 ◽  
Vol 74 (5) ◽  
pp. 2087-2099 ◽  
Author(s):  
L. Ris ◽  
C. de Waele ◽  
M. Serafin ◽  
P. P. Vidal ◽  
E. Godaux
Keyword(s):  
Guinea Pig ◽  
Vestibular Nucleus ◽  
Head Rotation ◽  
Second Order ◽  
Vestibular Nerve ◽  
Control Group ◽  
Head Velocity ◽  
Vestibular Neurons ◽  
Unilateral Labyrinthectomy ◽  
Control State

1. Neuronal activity was investigated in the left superior vestibular nucleus (SVN), lateral vestibular nucleus (LVN), and rostral part of the medial vestibular nucleus (MVN) in the alert guinea pig after a unilateral (left) labyrinthectomy was performed. Vestibular neurons were recorded either immediately (just-postoperative group, n = 6) or 1 wk after labyrinthectomy (1-wk-postoperative group, n = 6) and compared with the activity recorded in intact animals (control group, n = 6). 2. Animals were prepared for extracellular recording of single-unit activity and for eye movement recording (scleral search coil technique). To enable stimulation of the left vestibular nerve, bipolar silver ball electrodes were chronically implanted either in contact with the bony labyrinth in the control group or close to the stump of the vestibular nerve after labyrinthectomy. Complete labyrinthectomy was performed under halothane anesthesia. 3. The criterion used to select vestibular neurons for analysis was their recruitment by an electric shock on the vestibular nerve. Of the 589 recorded neurons, 424, defined as second-order vestibular neurons, were recruited at monosynaptic latencies (0.85-1.15 ms) and 165 were recruited at polysynaptic latencies. One hundred three second-order vestibular neurons were recorded in the control group, 173 in the just-postoperative group, and 148 in the 1-wk-postoperative group. 4. The activity of the electrically recruited neurons was recorded during sinusoidal horizontal head rotation in the dark (0.3 Hz, 40 degrees/s peak velocity). The behavior of the neurons was analyzed by plotting their firing rate against head velocity. The Y-intercept of the regression line was used to express spontaneous firing rate (resting discharge), and its slope was used to express the sensitivity of the neuron-to-head velocity. 5. In the absence of statistically significant difference between the characteristics of the neuronal discharge of the second-order vestibular neurons recorded in the SVN, LVN, and rostral MVN, the data were pooled. The Resting discharge of these cells amounted to 41.0 +/- 24.7 (SD) spikes/s in the control state, fell to 7.2 +/- 13.9 spikes/s just after labyrinthectomy, and completely returned to normal values 1 wk after surgery (42.5 +/- 21.6 spikes/s). Among the monosynaptically recruited neurons, the percentage of silent units was 0% in the control group, 69% in the just-postoperative group, and 0% in the 1-wk-postoperative group. 6. By contrast, the sensitivity to head velocity of the second-order vestibular neurons, which was 0.69 +/- 0.48 (SD) spikes.s-1/deg.s-1 in the control state and which fell to 0.03 +/- 0.11 spikes.s-1/deg.s-1 just after labyrinthectomy, remained low 1 wk after injury (0.21 +/- 0.26 spikes.s-1/deg.s-1). Moreover, the slight recovery of sensitivity to head rotation was due only to units behaving as type II neurons. 7. The mean resting discharge of the polysynaptically recruited neurons (pooled from the 3 explored nuclei) was 31.6 +/- 19.3 spikes/s in the control group. It decreased to 11.6 +/- 12.1 spikes/s in the just-postoperative group and recovered to 39.8 +/- 20.2 spikes/s in the 1-wk-postoperative group. No neuron was silent at rest either in the control group or in the 1-wk-postoperative group. Just after labyrinthectomy, 35% of the neurons had a null resting activity. The mean sensitivity to head velocity of these neurons was 0.55 +/- 0.42 spikes.s-1/deg.s-1 in the control group. It decreased to 0.05 +/- 0.12 spikes.s-1/deg.s-1 in the just-postoperative group and recovered to 0.22 +/- 0.17 spikes.s-1/deg.s-1 in the 1-wk-postoperative group. 8. We conclude that, at least in the guinea pig, the restoration of the spontaneous activity of the deafferented neurons is complete 1 wk after a unilateral labyrinthectomy and thus probably plays an important role in vestibular compensation...

Deafferentated vestibular nerve

1983 ◽  
Vol 41 ◽  
pp. 652-653
Author(s):  
C.D. Fermin ◽  
M. Igarashi
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Light Microscopy ◽  
Squirrel Monkey ◽  
Toluidine Blue ◽  
Vestibular Nerve ◽  
Saimiri Sciureus ◽  
Basic Fuchsin ◽  
Transmission Electron ◽  
Viiith Nerve

Contrary to the cochlear branch of the VIIIth nerve, the vestibular branch does not degenerate quickly in the squirrel monkey after the end organs are surgically removed. This surgical procedure is favored by some investigators who advocate that removal of the vestibular receptors does eventually lead to the death of the nerve. Others think that the neurons of the vestibular ganglion can regenerate and contribute to partial reoccurrence of the symptoms the patient had before surgery. Thus, this problem remains unsettled. We are presently studying the vestibular nerve and ganglia of the squirrel monkey (Saimiri sciureus) in order to examine the fate of the surviving neurons, and the changes that these cells undergo after labyrinthectomy. Animals were anesthetized, perfused intracardially and the specimens were processed for transmission electron microscopy (TEM) as previously described. For light microscopy (LM), some specimens were embedded in JB-4 plastic, cut serially at 5 micra and stained with 0.2% toluidine blue and 0.1% basic fuchsin in 25% alcohol.

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