Activity of "vestibular only" (VO) and "vestibular plus saccade" (VPS) units was recorded in the rostral part of the medial vestibular nucleus and caudal part of the superior vestibular nucleus of alert rhesus monkeys. By estimating the "null axes" of recorded units (n = 79), the optimal plane of activation was approximately the mean plane of reciprocal semicircular canals, i.e., lateral canals, left anterior-right posterior (LARP) canals or right anterior-left posterior (RALP) canals. All units were excited by rotation in a direction that excited a corresponding ipsilateral semicircular canal. Thus, they all displayed a "type I" response. With the animal upright, there were rapid changes in firing rates of both VO and VPS units in response to steps of angular velocity about a vertical axis. The units were bidirectionally activated during vestibular nystagmus (VN), horizontal optokinetic nystagmus (OKN), optokinetic after-nystagmus (OKAN) and off-vertical axis rotation (OVAR). The rising and falling time constants of the responses to rotation indicated that they were closely linked to velocity storage. There were differences between VPS and VO neurons in that activity of VO units followed the expected time course in response to a stimulus even during periods of drowsiness, when eye velocity was reduced. Firing rates of VPS units, on the other hand, were significantly reduced in the drowsy state. Lateral canal-related units had average firing rates that were linearly related to the bias or steady state level of horizontal eye velocity during OVAR over a range of +/- 60 deg/s. These units could be further divided into two classes according to whether they were modulated during OVAR. Non-modulated units (n = 5) were VO types and all modulated units (n = 5) were VPS types. There was no significant difference between the bias level sensitivities relative to eye velocity of the units with and without modulation (P > 0.05). The modulated units had no sustained change in firing rate in response to static head tilts and their phases relative to head position varied from unit to unit. The phase did not appear to be linked to the modulation of horizontal eye velocity during OVAR. The sensitivities of unit activity to eye velocity were similar during all stimulus modalities despite the different gains of eye velocity vs stimulus velocity during VN, OKN and OVAR. Therefore, VO and VPS units are likely to carry an eye velocity signal related to velocity storage.(ABSTRACT TRUNCATED AT 400 WORDS)
Recent theoretical multidimensional analyses of the vestibulo-ocular have described the transformations thought to be necessary to effect a specific eye motion in response to a given head motion in order to maintain gaze. Accordingly, components of the angular head velocity vector in the coordinate system representing the geometry of the semicircular canals are transformed into components of an angular eye velocity vector in the coordinate system representing the geometry of the extraocular muscles. The transformations themselves are thought to manifest connectivity and signal processing of the central nervous system. These theoretical analyses were based in part upon anatomical measurements of the geometry of the semicircular canals and extraocular muscles made in the human>5 rabbit:' and cat.'.'Blanks and co-workers assessed the orientation of semicircular canals in cats by both anatomical' and physiological9 means. An objective of the physiological study was to ascertain the "sensitivity vector" for individual semicircular canal afferents. The direction of the sensitivity vector for a particular afferent is the direction of the axis about which a given head angular rotation will maximally modulate that afferent's activity. In the physiological study9 data obtained from right semicircular canal afferents of many cats were averaged and compared with the anatomical data of the earlier study,' in which the bony portions of the semicircular canals on both sides of the head were measured in different animals and averaged. The two methods of
To clarify the role of the pretectal nucleus of the optic tract (NOT) in ocular following, we traced NOT efferents with tritiated leucine in the monkey and identified the cell groups they targeted. Strong local projections from the NOT were demonstrated to the superior colliculus and the dorsal terminal nucleus bilaterally and to the contralateral NOT. The contralateral oculomotor complex, including motoneurons (C-group) and subdivisions of the Edinger-Westphal complex, including motoneurons (C-group) and subdivisions of the Edinger-Westphal complex, also received inputs. NOT efferents terminated in all accessory optic nuclei (AON) ipsilaterally; contralateral AON projections arose from the pretectal olivary nucleus embedded in the NOT. Descending pathways contacted precerebellar nuclei: the dorsolateral and dorsomedial pontine nuclei, the nucleus reticularis tegmenti pontis, and the inferior olive. Direct projections from NOT to the ipsilateral nucleus prepositus hypoglossi (ppH) appeared to be weak, but retrograde tracer injections into rostral ppH verified this projection; furthermore, the injections demonstrated that AON efferents also enter this area. Efferents from the NOT also targeted ascending reticular networks from the pedunculopontine tegmental nucleus and the locus coeruleus. Rostrally, NOT projections included the magnocellular layers of the lateral geniculate nucleus (lgn); the pregeniculate, peripeduncular, and thalamic reticular nuclei; and the pulvinar, the zona incerta, the mesencephalic reticular formation, the intralaminar thalamic nuclei, and the hypothalamus. The NOT could generate optokinetic nystagmus through projections to the AON, the ppH, and the precerebellar nuclei. However, NOT also projects to structures controlling saccades, ocular pursuit, the near response, lgn motion sensitivity, visual attention, vigilance, and gain modification of the vestibulo-ocular reflex. Any hypothesis on the function of NOT must take into account its connectivity to all of these visuomotor structures.
Lesions were placed in the paramedian pontine reticular formation ( PPRF ) of monkeys and the resulting gaze palsies studied. Brainstem regions were identified by single cell recordings before kainic acid was injected to selectively destroy neuronal cell bodies in the vicinity. Unilateral PPRF lesions led to a loss of all rapid eye movements towards the ipsilateral side. Deficits were identical to those after experimental electrolytic lesions in monkeys, or structural lesions in humans. Bilateral PPRF lesions produced two different syndromes. Rostral PPRF lesions led to a selective loss of horizontal rapid eye movements leaving vertical movements intact. Caudal PPRF lesions led in addition to a severe disruption of vertical rapid eye movements.
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