Transcerebellar inhibitory interaction between the bilateral vestibular nuclei and its modulation by cerebellocortical activity

Summary In decerebrate, unanesthetized cats, the brain stem was longitudinally cut at the midline from its dorsal to ventral surface with the cerebellum kept intact, eliminating neural interactions between the bilateral vestibular nuclei through the brain stem.Extracellular spike potentials of vestibular type I neurons identified by horizontal rotation were distinctly inhibited by contralateral vestibular nerve stimulation. This crossed inhibition was abolished by removal of the medial part of the cerebellum, indicating that the inhibition was mediated through the cerebellum. Neither aspiration of the flocculus on the recording side nor intravenous administration of picrotoxin eliminated transcerebellar crossed inhibition, suggesting that it is mediated through the cerebellar nuclei. When the fastigial, interposite and dentate nuclei were stimulated, inhibition of vestibular type I neurons was produced only from the contralateral fastigial nucleus. Cerebellocortical stimulation which inhibited fastigial type I neurons suppressed transcerebellar crossed inhibition. Effective sites for suppression of transcerebellar crossed inhibition were localized to lobules VI and VIIa in the vermal cortex on the side of labyrinthine stimulation.Intracellular recordings were made from type I neurons in the medial vestibular nucleus. Stimulation of the contralateral vestibular nerve and the contralateral fastigial nucleus produced IPSPs in these neurons with the shortest latency of 3.8 msec and 1.8 msec, respectively. The difference between these two latency values approximates the shortest latency of spike initiation of fastigial type I neurons in response to vestibular nerve stimulation. It is postulated that transcerebellar crossed inhibition is mediated through the fastigial nucleus on the side of labyrinthine stimulation.     

Vestibular-evoked postsynaptic potentials in Deiters neurones

Summary Stimulation of the vestibular nerve induced EPSPs monosynaptically in 29% of cat's Deiters neurones sampled on the ipsilateral side. These EPSPs started with latencies of 0.6–1.0 msec, rose sharply with a summit time of 0.5 msec and decayed exponentially with a time constant of 0.9–1.7 msec. Then amplitudes were graded finely according to the intensity of the vestibular nerve stimulation, the maximal size being 5–10 mV. The unitary EPSPs, evoked by vestibular nerve stimulation at juxta-threshold intensity or appearing spontaneously, were as small as 0.2–0.3 mV in amplitude. Those neurones monosynaptically activated by vestibular nerve volleys were located in the ventral portion of the nucleus of Deiters, in agreement with histological data. The vestibular nerve impulses also produced delayed EPSPs with latencies of 1.0–1.8 msec, presumably disynaptically. They occurred in many Deiters neurones located not only ventrally but also dorsally. Even later EPSPs often were superposed on the monosynaptic EPSPs with latencies of 1.9–2.2 msec. There is evidence that they were caused by repetitive discharges in the vestibular nerve fibres which occur in response to single shock stimulation of the vestibular nerve. IPSPs were produced only polysynaptically in some Deiters neurones in association with the monosynaptic EPSPs.     

Projections of the group y of the vestibular nuclei and the dentate and fastigial nuclei of the cerebellum to the interstitial nucleus of Cajal

Experiments were performed to study the projection of the group y of the vestibular nuclei and the dentate and fastigial nuclei of the cerebellum to the interstitial nucleus of Cajal (INC) in cats by using retrograde axonal transport of horseradish peroxidase (HRP) and electrophysiological methods; and to study the vestibular responses of such projection neurons. Following injections of HRP into the unilateral INC, with partial involvement of the surrounding reticular formation, including the nucleus of Darkschewitsch (ND), many retrogradely labeled neurons were found in the dorsal part of the group y nucleus contralateral to the injection site. Labeled cells were also seen in the contralateral dentate nucleus, frequently in its caudal-ventral part, and in the contralateral fastigial nucleus at all rostrocaudal levels, but most frequently in its caudal part. In electrophysiological experiments performed on cats anesthetized with alpha-chloralose or N2O and paralyzed with gallamine, group y, dentate and fastigial nuclei neurons were antidromically activated by weak stimuli that were confined to the contralateral INC. Depth-threshold curves for antidromic activation of such neurons revealed that the lowest threshold points were within the INC, but not in the ND. The INC-projecting neurons in the group y and dentate nuclei did not respond to electrical stimulation of the ipsilateral or contralateral vestibular nerve, indicating that they do not receive direct labyrinthine inputs. On the contrary, many fastigial neurons projecting to the INC responded to labyrinthine stimulation, suggesting that they may be involved in the vestibular reflexes. These results suggest a difference in properties of INC-projecting neurons in these nuclei.     

The vestibulo-ocular reflex arc in the newborn kitten

Summary Field potentials and postsynaptic potentials were recorded in the vestibular and abducens nuclei and neurons following vestibular nerve stimulation in anesthetized newborn kittens (within 72 h after birth). Stimulation of the ipsilateral vestibular nerve evoked an initial P wave and an N₁ field potential in the vestibular nuclei. No N₂ potential was evoked. Latencies of the peak of the P wave, the onset and the peak of the N₁ potential were 0.99±0.16 ms, 1.66±0.18 ms, and 2.51±0.23 ms, respectively. Ipsilateral vestibular nerve stimulation evoked monosynaptic excitatory postsynaptic potentials (EPSPs) and polysynaptic inhibitory postsynaptic potentials (IPSPs) in vestibular nuclear neurons. Stimulation of the contralateral vestibular nerve evoked polysynaptic IPSPs in vestibular nuclear neurons. In abducens motoneurons, ipsilateral vestibular nerve stimulation evoked monosynaptic EPSPs and disynaptic IPSPs; contralateral vestibular nerve stimulation produced disynaptic EPSPs. We conclude that short circuit pathways of the vestibul-ovestibular and vestibulo-ocular reflex arc are present in the kitten already at birth.Supported by the Japanese Ministry of Education, Science, and Culture Grants-in-Aid for Scientific Research nos. 572 140 30 and 575 700 53     

Synaptic linkage in the vestibulo-ocular and cerebello-vestibular pathways to the VIth nucleus in the rabbit

Summary Intra- and extra-cellular responses were recorded with glass microelectrodes from motoneurons in the VIth cranial nuclei of anesthesized rabbits. VIth nucleus motoneurons were identified by their antidromic activation from the VIth nerve. In these motoneurons stimulation of the ipsilateral VIIIth nerve produced IPSPs with disynaptic latencies (mean and S.D., 1.08 ± 0.1 msec) while stimulation of the contralateral VIIIth nerve produced EPSPs with disynaptic latencies (mean and S.D., 1.20 ± 0.18 msec). Correspondingly, direct stimulation of the ipsilateral medial vestibular nucleus (MV), produced IPSPs with monosynaptic latencies (mean and S.D., 0.61±0.15 msec) while direct stimulation of the contralateral MV produced EPSPs with monosynaptic latencies (mean and S.D., 0.61±0.09 msec). Further, with the recording electrode placed within the VIth nucleus to observe the extracellular potentials corresponding to the intracellularly recorded IPSPs and EPSPs, the medulla was systematically tracked with a monopolar stimulating electrode. It was demonstrated that the inhibitory relay cells could be effectively stimulated in the rostral half of the ipsilateral MV and the excitatory relay cells in the rostral half of the contralateral MV.Pharmacological investigation suggested that the inhibitory transmitter involved in the vestibular inhibition is gamma amino-butyric acid or a related substance.Electric stimulation of the flocculus produced a prominant depression in the inhibitory vestibulo-ocular reflex pathway to the VIth nucleus, while the excitatory pathway was free of any similar flocculus inhibition.     

The effects of stimulating the cerebellar nodulus in the cat on the responses of vestibular neurons

In a first series of experiments, recordings were obtained from cat abducens and trochlear motorneurons and from axons of secondary vestibular neurons terminating in these motor nuclei, and the effects of cerebellar nodulus stimulation on utricular- and canal-evoked responses in these neurons were studied. Ultricular activation of vestibular axons recorded in the ipsilateral VIth and contralateral IVth nuclei was probably monosynaptically inhibited by nodular stimulation provided conditioning-test intervals were in the range between 0-10 ms and the test stimuli were close to threshold intensities. Of the vestibular axons activated by stimulation of the semicircular canal nerves only those evoked by the horizontal canal stimulation and recorded in the ipsilateral VIth nucleus were weakly inhibited. When the vestibular stimuli were strong enough to produce clear field potentials in the motor nuclei and/or postsynaptic potentials in motorneurons, nodular stimulation had practically no effect on their amplitudes. It is concluded that inhibition of vestibuloocular transmission is weak as compared to floccular inhibition studied previously. In a second series of experiments, recordings were obtained from vestibular neurons which were activated antidromically and/or transsynaptically by stimulation of the contralateral fastigial nucleus, and the effects of ipsilateral nodular stimulation on these responses were studied. It was found that nodular stimulation inhibited both antidromic as well as transsynaptic fastigial activations of vestibular neurons. Most of these vestibular neurons were located in the descending vestibular nucleus and received polysynaptic vestibular and spinal inputs. It is concluded that in addition to its weak inhibitory effect on vestibuloocular transmission the nodulus exerts a powerful inhibition on vestibular neurons transmitting vestibular and spinal inputs to cerebellar nuclei and/or cortex. It is suggested that the nodulus controls cerebellar projecting vestibular neurons which carry vestibular and spinal information to the cerebellum. The vestibular, proprioceptive and visual information which is present in the nodulus may aid the role of the nodulus in controlling body posture.     

Direct excitatory and inhibitory synaptic inputs from the medial mesodiencephalic junction to motoneurons innervating extraocular oblique muscles in the cat

Summary This study investigated the nature of synaptic inputs from the Forel's field H (FFH) in the medial mesodiencephalic junction to inferior oblique (IO) motoneurons in the oculomotor nucleus and superior oblique (SO) motoneurons in the trochlear nucleus in anesthetized cats, using intracellular recording techniques. Stimulation of the FFH induced monosynaptic EPSPs in IO motoneurons on both sides. Paired stimulation of the ipsilateral FFH and contralateral vestibular nerve substantiated that the FFH-induced EPSPs were caused mainly by direct excitatory fibers from the FFH to IO motoneurons and partly by axon collaterals of excitatory neurons in the vestibular nuclei. Among parts of the FFH, the medial part was most effective for producing the EPSPs. Systematic tracking with the stimulating electrode in and around the FFH revealed that effective sites of stimulation inducing negative field potentials in the IO subdivision of the oculomotor nucleus, identified as extracellular counterparts of the EPSPs in IO motoneurons, were also located in the interstitial nucleus of Cajal, nearby reticular formation and posterior commissure, besides within and near the medial part of the FFH. Areas far rostral, dorsal and ventral to the FFH were ineffective. EPSP-IPSPs or EPSPs were mainly induced in SO motoneurons on both sides by FFH stimulation. Latencies of these EPSPs and IPSPs were close to those of the EPSPs in IO motoneurons, indicating their monosynaptic nature. Effective stimulation sites for inducing these synaptic potentials overlapped those for the EPSPs in IO motoneurons. Based on these results, it was suggested that excitatory and inhibitory premotor neurons directly controlling IO and SO motoneurons were located within and near the medial part of the FFH.     

Convergence of posterior semicircular canal and saccular inputs in single vestibular nuclei neurons in cats

Convergence between posterior canal (PC) and saccular (SAC) inputs in single vestibular nuclei neurons was investigated in decerebrated cats. Postsynaptic potentials were recorded intracellularly after selective stimulation of the SAC and PC nerves. Stimulation of either the SAC or PC nerve orthodromically activated 143 vestibular nuclei neurons. Of these, 61 (43%) were antidromically activated by stimulation of the C1-C2 junction, 14 (10%) were antidromically activated by stimulation of the oculomotor or trochlear nucleus, and 14 (10%) were antidromically activated by stimulation of both the oculomotor or trochlear nucleus and the spinal cord. Fifty-four (38%) neurons were not activated by stimulation of either or both. We named these neurons vestibulospinal (VS), vestibulo-ocular (VO), vestibulooculo-spinal (VOS) and vestibular (V) neurons, respectively. Both PC and SAC inputs converged in 47 vestibular nuclei neurons (26 VS, 2 VO, 6 VOS and 13 V neurons). Of these, 19 received monosynaptic excitatory inputs from both nerves. This input pattern was frequently seen in VS neurons. Approximately half of the convergent VS neurons descended to the spinal cord through the lateral vestibulospinal tract. The remaining half and all the convergent VOS neurons descended to the spinal cord through the medial vestibulospinal tract. Most of the convergent neurons were located in the lateral nucleus or descending nucleus.     

Properties of utricular-activated vestibular neurons that project to the contralateral vestibular nuclei in the cat

The properties of utricular (UT)-activated vestibular neurons that send axons to the contralateral vestibular nuclei (commissural neurons) were investigated intracellularly or extracellularly in decerebrate cats. A total of 27 vestibular neurons were orthodromically activated by stimulation of UT nerves and antidromically activated by stimulation of the contralateral vestibular nuclei. All neurons tested were classified as vestibulospinal (VS), vestibulooculospinal (VOS), vestibuloocular (VO), and unidentified vestibular neurons (V) after antidromic stimulation of the spinal cord and oculomotor/trochlear nuclei. Most UT-activated commissural neurons (20/27) received monosynaptic inputs. Twelve of 27 commissural neurons were located in the medial vestibular nucleus, 5 were in the lateral vestibular nucleus, 10 were in the descending vestibular nucleus, and no commissural neurons were recorded in the superior vestibular nucleus. Seven of 27 neurons were commissural VS neurons, 9 of 27 were commissural VOS neurons, and 11 of 27 were commissural V neurons. No commissural VO neurons were found. All VOS neurons and 3 VS neurons issued descending axons via the medial vestibulospinal tract. We also studied convergent inputs from the posterior semicircular canal (PC) nerve onto UT-activated commissural neurons. Five of 27 UT-activated commissural neurons received converging inputs from the PC nerves. Electronic Publication     

Direct excitation of neck motoneurons by interstitiospinal fibers

1. Responses of neck motoneurons to stimulation of the interstitial nucleus of cajal (INC) were recorded intracellularly in cats under chloralose anesthesia. When stimuli were applied within or close to the INC, short latency, monosynaptic excitatory postsynaptic potentials (EPSPs) were evoked in many neck motoneurons. Such EPSPs were not evoked by stimulating mesencephalic regions outside the INC. 2. Stimulation of the ipsilateral INC produced monosynaptic EPSPs consistently in biventer cervicis-complexus (BCC) motoneurons, while such EPSPs were observed in about two thirds of the splenius (SP) motoneurons and half of the trapezius (TR) motoneurons tested. Stimulation of the contralateral INC produced weak monosynaptic EPSPs in about half the BCC motoneurons and in a few SP and TR motoneurons. All types of motoneurons also received longer latency, apparently polysynaptic, PSPs from both INCs. In BCC and TR motoneurons these were mainly EPSPs, in SP, mixed excitatory and inhibitory PSPs. 3. Monosynaptic EPSPs evoked by INC stimulation were not eliminated by acute and chronic parasagittal and transverse lesions placed to interrupt the bifurcating axons of all vestibulospinal and many reticulospinal neurons. No significant collision was observed between EPSPs evoked by INC and vestibular or reticular stimulation. The EPSPs evoked by stimulation of the INC therefore appear to have been produced by activation of interstitiospinal neurons rather than by an axon reflex mechanism. 4. The properties of a number of interstitiospinal neurons were observed while recording extracellularly from the mesencephalon to map the location of the INC. One third of the interstitiospinal neurons activated antidromically from the C4 segment could also be activated antidromically from L1. These lumbar-projecting neurons had conduction velocities ranging from 15--123 m/s. Several interstitiospinal neurons sending axons to the ventral horn of the neck segments were identified and two of these were found to be branching neurons that projected both to the neck and to lower levels of the spinal cord.     

Projections of vertical eye movement-related neurons in the interstitial nucleus of Cajal to the vestibular nucleus in the cat.

In two alert cats, single-unit activity of neurons related to vertical eye movement was recorded in and around the interstitial nucleus of Cajal (INC), and their projections to the ipsilateral vestibular nucleus and response to stimulation of the contralateral vestibular nerve were examined. Of 62 neurons that discharged in relation to vertical eye movement, 41 increased their firing rate for downward positions and 21 for upward positions. About one third of downward-on neurons was antidromically activated by stimulation of the ipsilateral vestibular nucleus with thresholds of 36-220 microA. None of the upward-on neurons were antidromically activated. About 60% of INC neurons (22/36) responded orthodromically to stimulation of the contralateral vestibular nerve. In particular, all the downward-on neurons that projected to the ipsilateral vestibular nucleus exhibited orthodromic responses at disynaptic latencies. The results, together with our previous finding that excitatory secondary vestibular neurons carrying vertical position signals project contralaterally to the INC, suggest that downward-on INC neurons receive direct connection from these secondary vestibular neurons and send the signals back to the ipsilateral vestibular nucleus. Interstitio-vestibular interactions through these pathways may be important in the generation of vertical eye position signals.     

Responses of neurons of lizard's,lacerta viridis,vestibular nuclei to electrical stimulation of the ipsi- and contralateral VIIIth nerves

Summary Field and intracellular potentials were recorded in the vestibular nuclei of the lizard following stimulation of the ipsi-and contralateral vestibular nerves. The field potentials induced by ipsilateral VIIIth nerve stimulation consisted of an early negative or positive-negative wave (presynaptic component) followed by a slow negativity (transsynaptic component). The spatial distribution of the field potential complex closely paralleled the extension of the vestibular nuclei. Mono- and polysynaptic EPSPs were recorded from vestibular neurons after ipsilateral VIIIth nerve stimulation. In some neurons early depolarizations preceded the EPSPs. These potentials may be elicited by electrical transmission. Often spikelike partial responses were superimposed on the EPSPs. It is assumed that these potentials represent dendritic spikes.Contralateral VIIIth nerve stimulation generated disynaptic and polysynaptic IPSPs in some neurons and EPSPs in others. The possible role of commissural inhibition in phylogeny is discussed.In a group of vestibular neurons stimulation of the ipsilateral VIIIth nerve evoked full action potentials with latencies ranging from 0.25–1.1 msec. These potentials are caused by antidromic activation of neurons which send their axons to the labyrinth.     

Excitatory input to burst neurons from the labyrinth and its mediating pathway in the cat: location and functional characteristics of burster-driving neurons

Summary 1. Spikes of single neurons were recorded extracellularly in the cat prepositus hypoglossi nucleus and the underlying reticular formation and were identified as type II neurons by horizontal rotation. Among these neurons, those activated by contralateral vestibular nerve stimulation with short latencies (1.5–3.0 ms) were selected for further study. 2. A class of these identified neurons was antidromically activated from the contralateral excitatory burst neuron (EBN) area immediately rostral to the abducens nucleus. Systematic tracking for antidromic stimulation revealed a wide distribution of effective spots in and near the EBN area, with varied latencies and thresholds, suggesting terminal branching in that area. The same neurons were also antidromically activated from the contralateral inhibitory burst neuron (IBN) area, the region near the midline, and the nucleus reticularis tegmenti pontis. 3. These neurons exhibited a characteristic firing pattern related to nystagmus: with contralateral rotation the firing rate gradually increased during the slow phase (type II response) and further steeply increased in a burst fashion before and during the contraversive quick phase. Since the time of occurrence of burst activity in these neurons was similar to that of contralateral ENBs and IBNs that received their axonal projection, it is suggested that they send excitatory input to burst neurons, and can thus be called burster-driving neurons (BDNs). 4. Intracellular study revealed that stimulation of the BDN area produced monosynaptic EPSPs in contralateral EBNs. The monosynaptic connection of BDNs with EBNs was confirmed by detecting unitary extracellular synaptic currents of EBNs with the spike-triggered averaging technique. 5. In contrast to BDNs, another class of nystagmus-related type II neurons in the prepositus hypoglossi and medullary reticular formation showed a discharge pattern similar to that of abducens motoneurons on the same side. None of them was antidromically activated from the contralateral pontine reticular formation including the EBN area. Some neurons responded anti-dromically to stimulation of the ipsilateral dorsomedial pontine reticular formation. 6. In conclusion, the input from the horizontal canal during rotation reaches the contralateral prepositus hypoglossi nucleus and the underlying reticular formation through the vestibular nuclei, and a class of neurons in these structures (BDNs) responds to the canal input in a burst fashion following a tonic type II activity. The axons of BDNs cross the midline and monosynaptically excite EBNs on the side of the canal stimulated. The burst activity of BDNs at the quick phase is suggested to contribute to generation of spike burst of EBNs and IBNs.     

Inhibitory reticular neurons related to the quick phase of vestibular nystagmus — Their location and projection

Summary The medial brain stem was explored mainly in the vicinity of the abducens nucleus to find interneurons related to the quick phase of vestibular nystagmus in the cat. Most neurons exhibiting a burst of spikes specifically at the quick phase of nystagmus directed to the ipsilateral side were found in the dorsomedial part of the reticular formation caudal to the abducens nucleus and lateral to the medial longitudinal fasciculus. The burst spikes were preceded by a negative field potential which was fairly localized in the above region. These neurons were activated antidromically from the contralateral and not from the ipsilateral abducens nucleus. The effective sites for antidromic activation showed a patch-like distribution in the abducens nucleus, indicating their axonal branching within the nucleus.Simultaneous recording of spikes of these neurons and the field potential in the contralateral abducens nucleus showed that a spike burst of each neuron began fairly synchronously with the onset of steep positive field potential in the abducens nucleus at the quick inhibitory phase of motoneurons. Microstimulation at the region where these neurons were located induced monosynaptic IPSPs in the contralateral abducens motoneurons. It is thus postulated that these neurons are inhibitory in nature and cause the IPSPs in contralateral abducens motoneurons at the quick inhibitory phase of vestibular nystagmus. The burst inhibitory neurons were activated polysynaptically from the ipsilateral vestibular nerve and monosynaptically from the contralateral superior colliculus or the ipsilateral pontine reticular formation at the level of P2–P6.     

Otolith-activated vestibulothalamic neurons in cats

The components of the vestibular ascending pathway that transmit otolith information to the thalamus were studied electrophysiologically in anesthetized cats. Thalamic-projecting vestibular neurons (confirmed antidromically) were recorded extracellularly in the various vestibular nuclei. Otolith inputs to these neurons were examined with selective stimulation of the utricular (UT) or the saccular (SAC) nerves. Vestibular nerve branches other than the tested nerve were transected. Of 40 UT-activated vestibulothalamic neurons, 40% (16/40) were activated by UT nerve stimulation with latencies ranging between 0.9-1.4 ms, suggesting they were second-order neurons from the UT nerve. UT-activated vestibulothalamic neurons were recorded in the medial vestibular nucleus (MVN; 24/40), the lateral vestibular nucleus (LVN; 9/40), the descending vestibular nucleus (DVN; 6/40), and the superior vestibular nucleus (SVN; 1/40). Most of the neurons (38/40) were antidromically activated by focal stimulation of the ventral part of the ipsilateral thalamus. Antidromic stimulation of the pontine area revealed that trajectories of the ascending axons (14 of 38 neurons) to the ipsilateral thalamus passed through the pontine reticular formation, ventral to the ascending tract of Deiters (ATD) and the medial longitudinal fasciculus (MLF). Only three SAC-activated vestibulothalamic neurons were encountered in the LVN. All these neurons were second-order neurons from the SAC nerve and were antidromically activated by stimulation of the contralateral thalamus, in marked contrast to the UT-activated vestibulothalamic neurons. Only three UT-activated and two SAC-activated neurons sent descending collaterals to the spinal cord.     

Direct projections from vestibular nuclei to facial nucleus in cats

Postsynaptic potentials were recorded from motoneurons in the facial nucleus in response to stimulation of the vestibular and trigeminal nerves. The motoneurons were identified by antidromic activation from their peripheral axons. Disynaptic excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) and mixed EPSP/IPSPs were recorded in response to vestibular nerve stimulation, ranging in latency from 0.9 to 2.1 ms, with most at 1.5 ms. Activity in secondary vestibular axons recorded within the facial nucleus occurred at a latency of 0.7-1.1 ms. The amplitudes of the vestibular postsynaptic potentials were small, generally less than a millivolt, but double shocks produced marked summation. The average time to peak of ipsilateral vestibular EPSPs, 1.1 ms, was faster than that of either ipsilateral IPSPs, 1.6 ms, or contralateral EPSPs, 1.4 ms. The double-spiked vestibular activity was detectable in double-peaked PSPs. Disynaptic EPSPs, ranging in latency from 2.0 to 3.0 ms, were recorded in response to trigeminal nerve stimulation. The average time to peak was 1.3 ms. The multiple-spiked activity of the trigeminal neurons was detectable in multipeaked EPSPs. Inhibitory ipsilateral effects (Vi IPSPs) were recorded twice as often as excitatory ipsilateral effects (Vi EPSPs), being found in 29% versus 15% of the motoneurons. Contralateral effects were found in 13% of the motoneurons studied, and almost all were excitatory. Analysis of synaptic potential shapes suggested that the excitatory and inhibitory vestibular synapses probably contact distal dendrites preferentially, with the excitatory connections being somewhat closer to the soma. The trigeminal inputs probably contact the facial motoneurons more extensively near the soma. Horseradish peroxidase was injected into the facial nucleus, and retrograde uptake by vestibular neurons was studied. The majority of filled vestibular neurons was ipsilateral to the injection site, especially in the medial vestibular nucleus, ventral y group, and supravestibular nucleus. On the contralateral side, filled vestibular cells were found almost exclusively in the medial nucleus. Filled cells were also noted in the trigeminal nucleus, predominantly ipsilaterally at all rostrocaudal levels. We have demonstrated monosynaptic projections to facial motoneurons from both vestibular and trigeminal nuclei. The trigeminal input is likely to be involved in facial reflexes, especially blinking and grimacing. The afferent vestibular population overlaps that going to the oculomotor and cervical motoneurons; these projections may be collaterals of single vestibular neurons.4+.     

Intracellular study of frog's vestibular neurons in relation to the labyrinth and spinal cord

Summary Field and intracellular potentials were recorded in the vestibular nuclei of the frog following stimulation of the anterior branch of the ipsilateral vestibular nerve and the spinal cord. The field potential induced by stimulation of the vestibular nerve consisted of an early positive-negative wave followed by a slow negativity and that recorded during spinal cord stimulation was composed of an antidromic potential followed by a slow negative wave. These potentials were most prominent in the ventral region of the stato-acoustic complex. Mono- and polysynaptic EPSPs were recorded from vestibular neurons following vestibular nerve stimulation. Short latency depolarizations of small amplitude preceded the monosynaptic EPSPs in some neurons. Spike-like partial responses were commonly superimposed on the EPSPs. These all-or-none depolarizations probably originated in the dendrites. In a group of vestibular neurons stimulation of the vestibular nerve evoked full action potentials with latencies ranging from 0.2 to 1.1 msec. They are presumably caused by antidromic activation of neurons which send their axons to the labyrinth. The presence of efferent neurons in the vestibular nuclei was confirmed by their successful staining with Procion Yellow following axonal electrophoresis.After stimulation of the spinal cord, antidromic spike potentials and EPSPs were recorded in vestibular neurons. In addition, short-latency depolarizing potentials (EDPs) were evoked by spinal stimulation, with latencies similar to those of antidromic potentials. The EDPs are suggested to be induced by electrotonic transmission from the neighboring cell and likely to be active spike potentials produced at some distance away from the soma.     

Input of anterior and posterior semicircular canal interneurons encoding head-velocity to the dorsal Y group of the vestibular nuclei

Neurons in the Y group of the vestibular nuclei are activated disynaptically from the ipsilateral VIIIth nerve and polysynaptically from the contralateral nerve. The ipsilateral anterior and posterior semicircular canals project to the Y group via interneurons in the vestibular nuclei. Candidate interneurons located in the rostrolateral corner of the superior (SVN) and in the caudal medial (MVN) vestibular nuclei were retrogradely labeled by the iontophoretic injection of biocytin into the Y group. The physiology of these interneurons named Y-group projecting neurons (YPNs) was studied in the SVN. SVN-YPNs were activated antidromically by electric pulse stimulation in the Y group. The properties of SVN-YPNs are distinct from those of SVN flocculus projecting neurons (FPNs). Namely, YPNs have a lower resting rate than FPNs, have more irregular interspike intervals, show a different phase and gain during the vestibuloocular reflex, and are located differentially within the SVN. After the injection of biocytin into the Y group, the locations of Purkinje cells that project to the Y group were confined to the vertical zones of the flocculus and ventral paraflocculus. However, mossy fibers originating in the Y group terminate in both the vertical and horizontal zones of the flocculus and ventral paraflocculus as well as in the ipsilateral nodulus.     

Fastigial nucleus projections to the brain stem in beagles: Pathways for autonomic regulation

Efferent connections from a portion of the cerebellar fastigial nucleus were investigated using autoradiography. Bipolar stimulating electrodes were placed in the fastigial nucleus of anesthetized beagles and the area that produced increases in blood pressure and heart rate was localized. A mixture of [³H]leucine and [³H]proline (4:1) was injected into the area and autoradiograms of transported material were prepared. Injections filled the rostral and various parts of the caudal fastigial nucleus. Labeled axons reached the brain stem via two routes, the ipsilateral juxtarestiform body and the contralateral uncinate fasciculus. Ventral portions of the lateral vestibular nucleus were labeled bilaterally, projections to the inferior vestibular and medial vestibular nuclei are contralateral. Nucleus tractus solitarius was heavily labeled on the side opposite the injection. The contralateral medial reticular formation contained many labeled terminals and axons. Label was found in the nucleus reticularis ventralis, lateral reticular nucleus, nucleus gigantocellularis, nucleus pontis caudalis and the paramedian reticular nucleus. No terminal labeling was found in nucleus parvocellularis or nucleus ambiguus.Stimulation of the rostral fastigial nucleus produces increases in blood pressure and heart rate by generalized sympathoexcitation. Many cell groups which facilitate the activity of preganglionic sympathetic neurons do not receive direct fastigial input. It is suggested that sympathoexcitation resulting from stimulation of the fastigial nucleus occurs through multisynaptic connections in the brain stem.     

Axon collaterals of anterior semicircular canal-activated vestibular neurons and their coactivation of extraocular and neck motoneurons in the cat

We studied the ascending and descending axonal trajectories of excitatory vestibular neurons related to the anterior semicircular canal, by means of local stimulation and spike-triggered signal averaging techniques in anesthetized cats. More than 200 vestibular neurons related to the ampullary nerve of the anterior semicircular canal (ACN) were identified as vestibulo-ocular neurons by antidromic stimulation of the contralateral inferior oblique (IO) muscle motoneuron pool. In the descending, medial and ventral lateral nuclei, about 60% of these vestibulo-ocular neurons were also activated antidromically by upper cervical spinal cord stimulation (vestibulo-ocular-collic (cervical) = VOC). These VOC neurons produced unitary EPSPs in the majority of neck extensor motoneurons located at the C₁ segment. None of the VOC neurons had axons descending as far as the thoracic level. Most of these VOC neurons were activated monosynaptically following stimulation of the ACN. The conduction velocity of the descending axons of VOC neurons was approximately 63 m/s, which was significantly faster than that of the ascending axons. The remaining 40% of the vestibulo-ocular neurons were not activated antidromically following spinal cord stimulation at intensities of 1 mA or more (vestibulo-ocular = VO). Most of the VO neurons were activated polysynaptically by ACN stimulation. The superior vestibular nucleus contained VO neurons that were activated mono- and polysynaptically following ACN stimulation.