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Monosynaptic activation of long descending propriospinal neurons from the lateral vestibular nucleus and the medial longitudinal fasciculus.

In decerebrate cats long descending propriospinal (LDP) neurons were recorded extracellularly in the cervical enlargement. They were identified antidromically by spinal cord stimulation at the L1-L2 level. Inputs to these cells were tested by stimulating the medial longitudinal fasciculus (MLF) 5 to 6 mm rostral to the obex, the lateral vestibular nucleus (LVN), the upper MLF 1 mm caudal to the trochlear nucleus, and the medial vestibular nucleus (MVN), all on the ipsilateral side. Action potentials were elicited in 44% (64/144) of LDP neurons in the ventral horn (laminae VII, VIII) at a segmental latency of 1 ms or less following brain stem stimulation. This was considered to be a monosynaptic latency. The most effective stimulation sites were the MLF and the LVN. MLF stimulation accounted for about two-thirds of the monosynaptically elicited action potentials and LVN for about one-third. Another 22% of LDP neurons responded at longer latencies, but some of those responses may also have been monosynaptic. Stimulation of the upper MLF and the MVN were much less effective, indicating that the MLF input was predominantly from fibers originating in the medullary and/or pontine reticular formation.

Animals↗

Vestibular ampullar modulation of hypoglossal neurons.

This paper describes preliminary observations on vestibular ampullar involvement in the control mechanism of the hypoglossal nucleus activity. Thermic stimulation of the labyrinth, performed by irrigating the external auditory meatus with cold water (20 degrees C), significantly modified the spontaneous electrical activity of hypoglossal neurons localized in the medio-caudal part of the nucleus. Tonic spontaneous discharge of the units following labyrinthine stimulation was modified into a phasic activity and bursts with multi-unit recruitment appeared. This modified activity was observed during 5-6 minutes after the onset of ear irrigation. Similar response patterns, but with shorter duration, were recorded following contralateral stimulation of the labyrinth. These results show that hypoglossal neurons are triggered by the vestibular system following dynamic conditions in response to every spatial head displacement.

Animals↗

Changes in responses of medial pontomedullary reticular neurons during repetitive cutaneous, vestibular, cortical, and tectal stimulation.

1. In cats anesthetized with chloralose, responses of medial pontomedullary reticular neurons to stimulation of the body surface, vestibular nerves, superior colliculi, pericruciate cortices, cerebral peduncles, and spinal cord were studied at different stimulus rates. Raising the rate from 1/10 s to between 1/4 s and 2/s caused a significant decrement or increment in the response of most neurons tested. Response decrement typically began near the beginning of the higher frequency stimulus sequence and increased throughout the sequence. Response increment usually began somewhat later, rose to a peak, and then declined. Recovery from response decrement or increment usually occurred within 30-60 s at a 1/10 s stimulus rate.2. Measurements of response latency and of changes occurring in the initial and longer latency portions of responses indicated that all components of a response typically decreased or increased in parallel. Background spontaneous activity did not change during response decrements, but sometimes increased during response increment.3. Where changes could be detected, response decrement usually developed more rapidly when a sequence of repetitive stimulation was repeated.4. Response decrement was most pronounced at the highest stimulation rates and lowest stimulus intensities. Response increment was usually maximal at a stimulus rate of 1/s: at lower rates less increment occurred; at higher rates responses began to exhibit decrement.5. Response changes varied with the type of stimulus applied. Response decrements predominated when the body surface, vestibular nerves, or ipsilateral superior colliculus were stimulated. Approximately equal amounts of response increment and decrement were produced by repetitive stimulation of the cerebral peduncles and contralateral superior colliculus. Stimulation of the surface of the pericruciate cortex or of the spinal cord usually produced a long-lasting response increment.6. Generalization of response decrement and increment was observed in cases where trains of stimuli at a rate of 2/s applied to one point produced changes in the response to stimulation of another point which was tested once per 10 s and where single-shock stimulation of the first point was without effect on the test response. Generalization of response decrement occurred most often when two nearby points were stimulated. Generalization of response increment appeared to spread widely between distant cutaneous points and stimuli of different kinds.7. The response decrement and increment observed in medial pontomedullary reticular neurons displayed most of the parametric features of behavioral habituation and sensitization (8, 33) and therefore appear to represent neural analogs of these latter phenomena. The properties of response decrement suggest that it may occur to a large extent within afferent pathways leading to medial reticular neurons...

Animals↗

Phasic modulation of transmission from vestibular inputs to reticulospinal neurons during fictive locomotion in lampreys.

The aim of this study was to determine whether the transmission from sensory inputs to reticulospinal neurons is modulated during fictive locomotion in lampreys. Reticulospinal neurons play a key role in the control of locomotion; modulation of sensory transmission to these neurons might be of importance for the adaptation of the control they exert during locomotion. In this series of experiments, intracellular synaptic responses of reticulospinal neurons of the posterior rhombencephalic reticular nucleus elicited by electrical stimulation of vestibular nerves on each side were studied during fictive locomotion induced by 50 microM N-methyl-D-aspartate (NMDA). Interestingly, shortly after NMDA had reached the bath and much before locomotor discharges were apparent in the recorded ventral roots, there was a significant depression of the synaptic transmission from vestibular nerves. The effect was reversed by washing out the NMDA and persisted in the isolated brainstem after spinal transection at the first segmental level. As locomotor discharges appeared in the ventral roots, synaptic responses elicited by vestibular nerve stimulation showed a clear phasic modulation of their amplitude during the locomotor cycle. Responses to stimulation of the ipsilateral vestibular nerve were smaller during the ipsilateral burst discharge than during the contralateral activity, whilst responses to stimulation of the contralateral vestibular nerve were minimal during contralateral activity and maximal during ipsilateral activity. This opposite pattern of modulation observed in the same reticulospinal neuron suggests that the phasic modulation of vestibular transmission is not due to changes in the membrane properties of the reticulospinal cell but is produced at a pre-reticular level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Interdependence of spatial properties and projection patterns of medial vestibulospinal tract neurons in the cat.

Activity of vestibular nucleus neurons with axons in the ipsi- or contralateral medial vestibulospinal tract was studied in decerebrate cats during sinusoidal, whole-body rotations in many planes in three-dimensional space. Antidromic activation of axon collaterals distinguished between neurons projecting only to neck segments from those with collaterals to C6 and/or oculomotor nucleus. Secondary neurons were identified by monosynaptic activation after labyrinth stimulation. A three-dimensional maximum activation direction vector (MAD) summarized the spatial properties of 151 of 169 neurons. The majority of secondary neurons (71%) terminated above the C6 segment. Of these, 43% had ascending collaterals to the oculomotor nucleus (VOC neurons), and 57% did not (VC neurons). The majority of VOC and VC neurons projected contralaterally and ipsilaterally, respectively. Most C6-projecting neurons could not be activated from oculomotor nucleus (V-C6 neurons) and projected primarily ipsilaterally. All VO-C6 neurons projected contralaterally. The distributions of MADs for secondary neurons with different projection patterns were different. Most VOC (84%) and contralaterally projecting VC (91%) neurons had MADs close to the activation vector of a semicircular canal pair, compared with 54% of ipsilaterally projecting VC (i-VC) and 39% of V-C6 neurons. Many i-VC (44%) and V-C6 (48%) neurons had responses suggesting convergent input from horizontal and vertical canal pairs. Horizontal and vertical gains were comparable for some, making it difficult to assign a primary canal input. MADs consistent with vertical-vertical canal pair convergence were less common. Type II yaw or type II roll responses were seen for 22% of the i-VC neurons, 68% of the V-C6 neurons, and no VOC cells. VO-C6 neurons had spatial properties between those of VOC and V-C6 neurons. These results suggest that secondary VOC neurons convey semicircular canal pair signals to both ocular and neck motor centers, perhaps linking eye and head movements. Secondary VC and V-C6 neurons carry more processed signals, possibly to drive neck and forelimb reflexes more selectively. Two groups of secondary i-VC neurons exhibited vertical-horizontal canal convergence similar to that present on neck muscles. The vertical-vertical canal convergence present on many neck muscles, however, was not present on medial vestibulospinal neurons. Spatial transformations achieved by the vestibulocollic reflex may occur in part on secondary neurons but further combination of canal signals must take place to generate compensatory muscle activity.

Animals↗

Vestibulotrigeminal and vestibulospinal projections in rats: retrograde tracing coupled to glutamic acid decarboxylase immunoreactivity.

Immunohistochemical experiments were performed using glutamic acid decarboxylase (GAD) to identify gamma-aminobutyric acid (GABA)ergic neurons in the vestibular nuclei (VN). VN neurons projecting to the sensory trigeminal complex (STC) or to the C1-C2 segments of the spinal cord were identified by injection of wheat germ agglutinin-apo-horseradish peroxidase coupled to colloidal gold (gold-HRP), a retrogradely transported tracer, in these structures. The experiments combining injection of gold-HRP in spinal cord and GAD immunohistochemistry revealed the existence in the medial, inferior and lateral VN of GAD immunoreactive neurons projecting to the spinal C1-C2 level. Experiments combining injection of gold-HRP in the STC and GAD immunohistochemistry demonstrated that, at least, 30-50% of the vestibulo-trigeminal neurons also contained GAD. Injections of two different retrograde tracers (gold-HRP and Biotinylated dextran amine) in the STC and the spinal cord demonstrated that some VN neurons project by axon collaterals to both structures. Because of the GABAergic spinal and STC vestibular projections we assume that these VN neurons with collateral projection are GABAergic. Therefore primary afferents from the face, neck or hindlimb could be modulated by inhibitory influences from GABAergic vestibular neurons.

Animals↗

Transformation of vestibular signals into motor commands in the vestibuloocular reflex pathways of monkeys.

Parallel pathways mediate the rotatory vestibuloocular reflex (VOR). If the VOR undergoes adaptive modification with spectacles that change the magnification of the visual scene, signals in one neural pathway are modified, whereas those in another are not. By recording the responses of vestibular afferents and abducens neurons for vestibular oscillations at frequencies from 0.5 to 50 Hz, we have elucidated how vestibular signals are processed in the modified versus unmodified VOR pathways. For the small stimuli we used (+/- 15 degrees/s), the afferents with the most regular spontaneous discharge fired throughout the cycle of oscillation even at 50 Hz, whereas afferents with more irregular discharge showed phase locking. For all afferents, the firing rate was in phase with stimulus head velocity at low frequencies and showed progressive phase lead as frequency increased. Sensitivity to head velocity increased steadily as a function of frequency. Abducens neurons showed highly regular spontaneous discharge and very little evidence of phase locking. Their sensitivity to head velocity during the VOR was relatively flat across frequencies; firing rate lagged head velocity at low frequencies and shifted to large phase leads as stimulus frequency increased. When afferent responses were provided as inputs to a two-pathway model of the VOR, the output of the model reproduced the responses of abducens neurons if the unmodified and modified VOR pathways had frequency-dependent internal gains and included fixed time delays of 1.5 and 9 ms. The phase shifts predicted by the model provide fingerprints for identifying brain stem neurons that participate in the modified versus unmodified VOR pathways.

Acoustic Stimulation↗

Bilateral processing of vestibular responses revealed by injecting lidocaine into the eighth cranial nerve in vitro.

Extracellular unit responses were recorded from the vestibular nucleus (VN) and medial longitudinal fasciculus during horizontal head rotation of an in vitro turtle brainstem in which the temporal bones remained attached. Units were characterized as type I or type II based on the responses to ipsiversive or contraversive rotation, respectively. Lidocaine injections (0.5-2 microl of 0.5%) into the root of the eighth cranial nerve within the cranium caused rapid effects on unit responses to head rotation. Responses of type I units were reduced by ipsilateral injection but enhanced following contralateral injection. On the other hand, type II units had their responses increased by ipsilateral injections yet decreased by contralateral injections. In approximately half of the type II cells, decrease of the contraversive response was accompanied by the appearance of latent ipsiversive activity. Our findings not only confirm that each eighth nerve has afferents that drive ipsiversive excitation of both vestibular nuclei but also suggest that both nerves compete to dominate a central neuron's vestibular response. These results may be inconsistent with the push-pull vestibular model in which each nerve drives the central neuron with a complementary response that enhances the vestibular output. An alternate model is described in which vestibular neurons receive bilateral excitation, and that excitatory input is antagonized by crossed inhibition during contraversive motion.

Action Potentials↗

Parasolitary nucleus: a source of GABAergic vestibular information to the inferior olive of rat and rabbit.

At least two subnuclei of the inferior olive, the beta-nucleus, and the dorsomedial cell column (dmcc), contain vestibularly responsive neurons that receive a dense descending projection that uses gamma-aminobutyric acid (GABA) as the transmitter. In contrast to the GABAergic innervation of other olivary subnuclei, the terminal boutons that terminate on neurons in the beta-nucleus and the dorsomedial cell column remain intact after cerebellectomy, ruling out both the cerebellum and the cerebellar nuclei as afferent sources. By using both immunohistochemical as well as orthograde and retrograde tracer methods, we have identified the source of the GABAergic pathway to the beta-nucleus and dmcc in both rat and rabbit. Under physiologic recording of single olivary neurons to guide electrode placement, we injected the bidirectional tracer, wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) into the beta-nucleus and dmcc of the inferior olive. These injections retrogradely labeled neurons in the parasolitary nucleus (Psol) near the vestibular complex. Psol neurons were identified as GABAergic with an antibody to glutamic acid decarboxylase (GAD). In the rat, Psol neurons are small (5-7 microm in diameter) and number approximately 1,800. In the rabbit, they are slightly larger (6-9 microm in diameter) and number approximately 2,200. WGA-HRP injections in conjunction with GAD immunohistochemistry double labeled a high percentage of neurons in both the rat and rabbit Psol. Injection of the orthograde tracer Phaseolus vulgaris-leucoagglutinin into the area of the Psol revealed a projection from this region to both the beta-nucleus and dmcc. Subtotal electrolytic lesions of this division of the Psol caused a substantial reduction in GAD-positive synaptic terminals in both the ipsilateral beta-nucleus and dmcc. The location of these GABAergic neurons, bordering both the nucleus solitarius and caudal vestibular complex, emphasizes the importance of the Psol in the processing of both vestibular and autonomic information pertinent to postural control.

Animals↗

Inhibitory effects of motilin, somatostatin, [Leu]enkephalin, [Met]enkephalin, and taurine on neurons of the lateral vestibular nucleus: interactions with gamma-aminobutyric acid.

Motilin, [Met]enkephalin, [Leu]enkephalin, somatostatin, taurine, gamma-aminobutyric acid (GABA), and glycine were tested for their effects on Deiters neurons of the lateral vestibular nucleus in rabbits. Iontophoresis was carried out with multibarrelled micropipettes. All four peptides and three amino acids produced depression of neuron firing. No facilitatory responses were observed. The depressant action of each peptide when iontophoresed alone was dose-dependent and was rapid in onset and recovery. Their characteristic actions suggest the possibility of their independent roles as strong inhibitors, although the experimental paradigm does not allow conclusions about the individual potency of each peptide. When GABA was administered together with motilin, [Met]enkephalin, or somatostatin, the effects of the peptide and GABA were additive, producing depression greater than that with application of either substance alone. When GABA was applied in conjunction with [Leu]enkephalin, more complex interactions were observed. At low iontophoretic currents, [Leu]enkephalin antagonized the action of GABA, producing a depression less than that of GABA alone and of considerably slower onset, suggesting an additional modulatory effect. These observations support the conclusion that all substances tested are chemical mediators in the lateral vestibular nucleus and [Leu]enkephalin may be a neuromodulator as well. Because recent immunocytochemical studies indicate that Purkinje cells in the cerebellar cortex are chemically heterogeneous and exhibit immunoreactivity for motilin, taurine, the enkephalins, and somatostatin, as well as for the GABA-synthesizing enzyme glutamic acid decarboxylase, it is suggested that the Purkinje cell projections to vestibular and cerebellar nuclei are multimodal in their chemical coding. The uniformly depressant action of the peptides and amino acids reported here is consistent with earlier observations that Purkinje cells exert an inhibitory influence on the vestibular and central cerebellar nuclei.

Action Potentials↗

Evidence that perihypoglossal neurons involved in vestibular-auditory and gaze control functions respond to nerve growth factor.

Nerve growth factor (NGF), which has long been considered to be a trophic factor for peripheral sensory and sympathetic neurons, has been found recently to influence cholinergic neurons in the basal forebrain and neostriatum. In the present study, we provide evidence that brainstem neurons in the perihypoglossal area that relay information from the inner ear and vestibular apparatus to the cerebellum and tectum are responsive to NGF. These neurons, which are located in the nucleus prepositus hypoglossi (NPH), spinal vestibular nucleus, cochlear complex, and gigantocellular and paragigantocellular nuclei of the reticular formation, express functional receptors for NGF and up-regulate the expression of trkA receptors after injection of NGF into targets. In addition, the developmental up-regulation of NGF in the cerebellum coincides with the differentiation of the perihypoglossal nuclei. These results suggest that neurons representing the principal brain relays for auditory and vestibular pathways and perihypoglossal neurons involved in gaze coordination are a novel group of central neurons (besides cholinergic neurons in the basal forebrain and neostriatum) that respond to NGF.

Animals↗

Response characteristics of neurons in the cat vestibular nuclei during slow and constant velocity off-vertical axes rotations in the clockwise and counterclockwise rotations.

The responses to slow constant velocity rotations in the clockwise (CW) and counterclockwise (CCW) directions about an axis tilted 10 degrees from the earth's vertical were studied in static tilt-sensitive neurons in the vestibular nuclei of decerebrate cats. Each unit responded to any 360 degrees unidirectional rotation with a position-dependent discharge maximum. The location of the maximum, obtained by rotation in one direction, differed from that obtained by an oppositely directed rotation (phase difference). In about 80% of the units such phase difference (up to 160 degrees in second-order neurons) in response to oppositely directed rotations was unaffected by different amplitudes of head displacement (5-25 degrees). Units were thus classified into two groups depending on the location of the CW discharge maximum relative to the CCW counterpart. The direction of rotation had no influence on the response gains of these units.

Animals↗

Characteristicas and response differences to iontophoretically applied norepinephrine, D-amphetamine and acetylcholine on neurons in the medial and lateral vestibular nuclei of the cat.

Midcollicular decerebrate cats, with their cerebellum removes, were tested with controlled acceleratory motion in order to identify neurons in the medial vestibular nucleus (MVN) and lateral vestibular nucleus (LVN) which responded to a motion stimulus. Five-barredled micropipettes were used to record single neuron activity and to apply norepinephrine (NE), d-amphetamine and acetylcholine (ACh). These agents were studied on spontaneously firing cells which responded to a motion stimulus and others which were in the MVN were inhibited by NE and d-amphetamine but were unaffected by iontophoresis of the alpha-adrenergic blocking agent phentolamine or the beta-antagonists, MJ-1999 or propranolol. In the LVN a majority of the cells tested were excited by NE and d-amphetamine. NE excitation in the LVN was antagonized by phentolamine but not by MJ-1999 or propranolo. Cats pretreated with reserpine to deplete brain catechlamines showed typical responses to NE BUT IONTOPHORESIS OF D-AMPHETAMINE WAS WITHOUT EFFECT. Unlike the differential sensitivity observed for NE, ACh excited most cells in both the MVN and LVN. NE and ACh produced similar responsed on vestibular neurons modulated by motion and those not responsive to motion. These observations suggest that NE-containing terminals are in close proximity to the vestibular neurons which were tested and further implicate both NE and ACh as neurotransmitters in afferent pathways to the vestibular nuclei.

Acetylcholine↗

Dissociations between behavioural recovery and restoration of vestibular activity in the unilabyrinthectomized guinea-pig.

1. In the guinea-pig, a unilateral labyrinthectomy induces postural disturbances and an ocular nystagmus which abate or disappear over time. These behavioural changes are accompanied by an initial collapse and a subsequent restoration of the spontaneous activity in the neurones of the ipsilateral vestibular nuclei. Recently, it has been shown that the vestibular neuronal activity remained collapsed over at least 10 h whereas its restoration was complete 1 week after the lesion. The aims of this study were to determine when restoration of spontaneous activity in the partially deafferented vestibular neurones started and to compare the time courses of the behavioural and neuronal recoveries in guinea-pigs that had undergone a unilateral labyrinthectomy. 2. Neuronal discharge measurements were made using chronic extracellular recording of single unit activity. After a left labyrinthectomy, electrodes, were placed on the site of the destroyed labyrinth to enable stimulation of the left vestibular nerve. Behavioural measurements included chronic recording of eye movements by the scleral search coli technique. After a left labyrinthectomy, lateral deviation of the head, twisting of the head, and eye velocity of the slow phases of the nystagmus were measured. 3. The neuronal activity of the rostral part of the vestibular nuclear complex on the lesioned side was recorded in alert guinea-pigs over 4 h recording sessions between 12 and 72 h after the lesion. 4. The criterion used to select vestibular neurones for analysis was their recruitment by an electric shock on the vestibular nerve. In addition, in order to explore a uniform population, we focused on neurones recruited at monosynaptic latencies (0.85-1.15 ms). 5. For each recording period, the mean resting rate was calculated animal by animal and the grand mean of these individual resting rate means was calculated. Previously, a decline in the grand mean resting rate from 35.8 +/- 6.0 spikes s-1 (control state) to 7.1 +/- 4.2 spikes s-1 during the first 4 h after labyrinthectomy has been shown. In the present study, the first sign of recovery was observed during the 12-16 h recording period when the resting rate grand mean increased to 16.3 +/- 3.9 spikes s-1. This grand mean activity did not change significantly during the following 12 h. Thereafter, restoration of neuronal activity improved and was complete 1 week after the lesion. 6. Although the abatement of the vestibular symptoms roughly paralleled the restoration of neuronal activity in the vestibular nuclei, some discrepancies between the time courses of both phenomena emerged. An important step in postural recovery (the animals managed to stand up) and a major part of the abatement of the nystagmus occurred before the recovery of vestibular neuronal activity. In addition, lateral deviation of the head disappeared while restoration of the neuronal activity was incomplete, but significant head twisting was still evident when vestibular resting rates had recovered completely. 7. We conclude that restoration of neuronal activity in the ipsilateral vestibular nuclei starts 12 h after the lesion and that restoration of neuronal activity in the ipsilateral vestibular nuclei is not the only mechanism underlying behavioural vestibular compensation.

Animals↗

Effects of stimulation of vestibular and neck receptors on Deiters neurons projecting to the lumbosacral cord.

The activity of lateral vestibular nucleus (LVN) neurons, antidromically identified by stimulation of the spinal cord at T12 and L1, thus projecting to the lumbosacral segments of the spinal cord (IVS neurons), was recorded in precollicular decerebrate cats during rotation about the longitudinal axis either of the whole animal (labyrinth input) or of the body only while the head was kept stationary (neck input). Among the IVS neurons tested for vestibular stimulation, 76 of 129 units (i.e. 58.9%) responded to roll tilt of the animal at the standard parameters of 0.026 Hz, +/- 10 degrees. The gain and the sensitivity of the first harmonic responses corresponded on the average to 0.47 +/- 0.44, SD, impulses X s-1 X deg-1 and 3.24 +/- 3.15, SD, %/deg, respectively. As to the response patterns, 51 of 76 units (i.e. 67.1%) were excited during side-down and depressed during side-up tilt, whereas 15 (i.e. 19.7%) showed the opposite behavior. In both instances the peak of the responses occurred with an average phase lead of about +21.0 +/- 27.2, SD, deg with respect to the extreme side-down or side-up position of the animal. Moreover, the former group of units showed almost a twofold larger gain with respect to the latter group (t-test, p less than 0.05). Among the IVS neurons tested for neck stimulation, 75 of 109 units (68.8%) responded to neck rotation at the standard parameters. The gain and the sensitivity of the first harmonic responses corresponded on the average to 0.49 +/- 0.40, SD, impulses X s-1 X deg-1 and 3.30 +/- 3.42, SD, %/deg, respectively, thus being similar to the values obtained for the labyrinth responses. However, 59 of 75 units (i.e. 78.6%) were excited during side-up neck rotation and depressed during side-down neck rotation, while 8 of 75 units (i.e. 10.7%) showed the opposite pattern. In both instances the peak of the responses occurred with an average phase lead of +52.0 +/- 18.3, SD, deg for the extreme side-up or side-down neck displacements. Further, the former group of units showed a larger gain than the latter group. Histological controls indicated that 102 of 129 (i.e. 79.0%) IVS neurons tested for labyrinth stimulation and 86 of 109 (i.e. 78.9%) IVS neurons tested for neck stimulation were located in the dorsocaudal part of LVN, the remaining IVS neurons being located in the rostroventral part of LVN.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

Postvibration changes in the spike activity of neurons in the medial vestibular nucleus.

Changes in the baseline spike activity in the medial vestibular nucleus were studied after exposure to vibration for 5, 10, and 15 days. Studies addressed the distributions of neurons within this structure in terms of the regularity of their spike activity, the dynamics of neural flows, and the modalities of interspike histogram modalities. Mean values were calculated for the major statistical measures of baseline spike activity. Statistically significant changes in the major characteristics of neuron activity were seen in the medial vestibular nucleus at different periods of vibration exposure. Vibration was found to induce complex dynamic rearrangements in the baseline activity of neurons in this structure. The characteristics and functional significance of the results are discussed.

Action Potentials↗

[Transformation of vestibular signals by cerebral cortical neurons in the cat].

Extracellular unit activity of cortical vestibular projections was recorded in wakeful, immobilized and artificially respirated cats. Natural vestibular stimulation included both sinusoidal and trapezoidal position profiles in the horizontal plane. Tonic and phasic neurons were discriminated. The responses of phasic neurons were direction-specific. The transformation of the vestibular signals by cortical neurons had quasilinear properties: linearity existed only in the velocity range from 0 to 30-50 deg.s-1. A conclusion is made that only a complex of responses of direction-specific neurons can give the full information about changes in the angular velocity.

Acceleration↗