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Notes: Summary (1) Spikes of neurons in the medial and descending vestibular nuclei were recorded extracellularly and their responses to stimulation of the interstitial nucleus of Cajal (INC) were studied in cerebellectomized cats under chloralose anesthesia. Stimuli applied in the ipsilateral INC excited 37% of neurons that did not exhibit spontaneous activity. About 84% of spontaneously discharging neurons were influenced by the INC; typical responses were excitation (35%), inhibition (22%) and excitation followed by inhibition (27%). Of the neurons that were excited, 24% fired monosynaptically. Such monosynaptic activation was evoked by stimulating the INC and midbrain medial longitudinal fasciculus (MLF), but was not evoked by stimulating the lateral midbrain reticular formation. Polysynaptic excitation or inhibition was evoked more widely, but the lowest threshold points were within the INC. Stimulation of the contralateral INC also evoked polysynaptic excitation or inhibition. However, the frequency of occurrence of the evoked responses was significantly smaller compared to the ipsilateral responses. (2) Intracellular recordings revealed that some medial and lateral vestibular neurons received monosynaptic excitatory postsynaptic potentials (EPSPs), others received polysynaptic EPSPs or inhibitory postsynaptic potentials (IPSPs) from the ipsilateral INC. The minimum latency for the IPSPs suggests that the pathway is at least disynaptic. No significant collision was observed between monosynaptic EPSPs evoked by the ipsilateral INC and contralateral vestibular nuclei. Acute lesions that damaged the pontine MLF and part of the reticular formation did not abolish monosynaptic responses of vestibular neurons by the INC. Depth threshold curves for mono- or polysynaptic responses drawn before and after the lesions were virtually similar. Antidromic thresholds of interstitio-vestibular fibers evoked from the pontine MLF showed that a great majority of these fibers run outside the MLF at the pontine level. These results control for vestibular axon reflexes, since vestibulo-interstitial fibers ascend within the MLF (cf. Gacek 1971). (3) Responses to stimulation of the INC were not different among different types of canal responding neurons; vertical and horizontal canal responding neurons received similar effects. However, canal responding neurons that received excitation from the contralateral vestibular nerve were activated more frequently by the INC than those that received inhibition (χ2 test, p〈0.01). Qualitatively similar results were obtained from vestibular neurons that had different projection sites; vestibulospinal, contralateral INC-projecting and contralateral vestibular nuclei-projecting neurons received similar effects. (4) Vestibulo-collic reflexes, studied with EMG, were modified by preceding INC stimulation. Intracellular recordings from some neck motoneurons showed that disynaptic EPSPs evoked by stimulation of the contralateral vestibular nerve were modified by preceding INC stimulation applied ipsilateral to the stimulated vestibular nerve. INC stimulation alone did not evoke any response in these motoneurons, suggesting that the interaction of the labyrinthine and interstitial effects occurred at least in part at the vestibular nuclei. (5) Some medial and descending vestibular neurons showed multiple branching, projecting to the contralateral INC, C1 or contralateral vestibular nuclei. About 34% of neurons that projected to the contralateral INC were also antidromically activated from the C1; some of them received vertical canal inputs.

Notes: Summary 1. Experiments were performed in cats to determine whether the head tilt following a unilateral lesion of the interstitial nucleus of Cajal (INC) can be attributed to removal of interstitiospihal fibers which have direct excitatory synaptic connections with ipsilateral neck extensor (biventer cervicis-complexus) and flexor (sternocleidomastoid, SCM) motoneurons. Unilateral INC lesions were made either electrolytically or reversibly by procaine infusion into the INC, and electromyographic activity was recorded bilaterally from biventer (BIV), splenius (SP) and SCM muscles. In both groups of lesions, activity of the ipsilateral SP and BIV was higher than that of the contralateral ones. When procaine was infused into the INC of awake cats, an increase of activity of the ipsilateral SP began before the cats presented the typical head tilt to the opposite side. Bilateral INC lesions caused dorsiflexion of the head. These results indicate that the head tilt resulting from unilateral INC lesions can not be explained by simple removal of the ipsilateral, direct excitatory interstitioneck impulses. 2. When unilateral INC lesions were combined with hemilabyrinthectomies, cats that were given labyrinthectomies on the side opposite to the previous INC lesions showed very severe head tilt, whereas cats that received labyrinthectomies on the same side did not show obvious head tilt. Furthermore, it took a much longer time for the cats of the former group to compensate the head tilt than it took those that had single lesions of the INC or labyrinth. These results suggest that the INC and labyrinth interact in the control of head posture and that the INC also plays a role in vestibular compensation. However, when bilatral INC lesions were combined with hemilabyrinthectomies, cats that had previously received bilateral INC lesions and which had fully compensated the head posture recuperated from vestibular symptoms following hemilabyrinthectomy within one to two weeks. Moreover, bilateral INC lesions that were performed in cats which had previously been given hemilabyrinthectomies and in which vestibular symptoms were well compensated did not produce any recurrence of vestibular symptoms. These results indicate that although the INC plays a role in the control of head posture following hemilabyrinthectomy, it is not needed for coarse vestibular compensation.

Notes: Summary 1. Experiments were performed in cats anesthetized with nitrous oxide to study the effects of INC lesions on responses of vestibular nuclear neurons during sinusoidal rotations of the head in the vertical (pitch) plane. Responses of neurons in the INC region were recorded during pitch rotations at 0.15 Hz. A great majority of these neurons did not respond to static pitch tilts, and they seemed to respond either to anterior or to posterior semicircular canal inputs with a peak phase lag of 140 deg (re head acceleration). 2. Responses of vestibular nuclei neurons in intact cats were recorded during pitch rotations at the same frequency (0.15 Hz). Neurons that seemed to respond to vertical semicircular canal inputs showed peak phase lags of 90 deg relative to head acceleration, whereas neurons that responded to static pitch tilts showed peak phase shifts near 0 deg. These results indicate that responses of neurons in the INC region lag those of vestibular neurons by about 50 deg, suggesting that the former neurons possess a phase-lagging (i.e. integrated) vestibular signal. 3. Responses of vestibular neurons in cats that had received electrolytic lesions of bilateral INCs 1–2 weeks previously were recorded during pitch rotations at the same frequency (0.15 Hz). Neurons that presumably responded to vertical semicircular canal inputs showed a peak phase lag of 60 deg relative to head acceleration, a significant decrease of the phase lag compared to normal, whereas responses near 0 deg were unchanged. Gain values of individual cells also significantly dropped from 2.07 ± 0.67 spikes · s−1/deg · s−22 (mean ± SD; normal cats) to 1.27 ± 0.68 spikes · s−2/deg · s−2 (INC lesioned cats) at 0.15 Hz. When responses of vestibular neurons were studied during pitch rotations in the range of 0.044–0.49 Hz in these cats, a large decrease of the phase lag was observed at lower frequencies, whereas the slopes of phase lag curves of vestibular neurons in intact cats were rather flat. 4. Procaine infusion into the bilateral INCs not only resulted in a decrease of 20–50 deg in the phase lag in responses of vestibular neurons that had lagged head acceleration by 90–140 deg before procaine infusion, but also dropped the gain of the response to rotation by an average of 31%, whereas responses of neurons that had showed phase shifts near 0 deg were not influenced consistently. Simultaneous recording of the vestibular neurons and the vertical vestibuloocular reflex (VOR) indicated that the phase advance and gain drop of vestibular neurons occurred earlier than those of the VOR. These results exclude the possibility that the change in dynamic response of vestibular neurons after procaine infusion is due to depression of general brain stem activity that may lead to the phase advance of the VOR, and suggest that the decrease of the phase lag and gain drop in responses of the vestibular neurons was caused by removal of the phase-lagging, feedback signal coming from the INC to the vestibular nuclei.