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Biomedical subjects

W Waespe

Publications and source records attributed to W Waespe.

At least 73 records · Page 4Linked to original sources
PubMed1983

Flocculectomy and unit activity in the vestibular nuclei during visual-vestibular interactions.

Activity of neurons in the vestibular nuclei of alert monkeys was recorded extracellularly after total unilateral and bilateral flocculectomy and partial paraflocculectomy. Type 1 horizontal cells that were encountered after flocculectomy responded to visual and vestibular stimuli and to conflict stimulation, i.e., to rotation in a subject-stationary visual surround, as do vestibular neurons in the normal animal. The major difference between neurons in the normal and lesioned animals was that more time was needed to reach steady state firing levels during optokinetic stimulation at a constant velocity after operation. As shown previously (Waespe et al. 1983) the longer time course is related to increased initial retinal slip velocities that occur after flocculectomy as a result of an inability to change eye velocity rapidly in response to visual stimulation. It does not signify a change in the dynamics of neurons in the vestibular nuclei that mediate the vestibulo-ocular reflex (VOR). The similarity in modulation of horizontal Type 1 vestibular neurons in normal and flocculectomized monkeys makes it unlikely that floccular Purkinje cells suppress the horizontal VOR in the monkey during conflicting visual and vestibular stimuli by inhibiting or disfacilitating secondary or tertiary vestibular neurons. This is consistent with earlier findings that indicate that visual-oculomotor pathways responsible for ocular pursuit or for rapid changes in OKN do not go through the vestibular nuclei. Rather the point of interaction of the flocculus output with the VOR appears to be external to the vestibular nuclei. There was a close correspondence between the slow phase velocity of nystagmus and unit activity in the vestibular nuclei under a wide variety of test conditions after flocculectomy. This is consistent with the postulate that frequencies of vestibular nuclei neurons represent a summation of activity in direct vestibulo-oculomotor pathways and indirect pathways that include the velocity storage mechanism. These are the major remaining sources of activity that generate slow phases of nystagmus after the direct visual-oculomotor pathways have been partially interrupted by flocculectomy (Waespe et al. 1983). Horizontal Type 1 neurons which responded to vestibular and optokinetic stimulation with increases in frequency above 1 spike/s/degree/s were rarely encountered after flocculectomy. These cells were present on the normal side in a monkey after unilateral flocculectomy. We infer that vestibular nuclei neurons that project mossy fibers to the flocculus are inactivated or disappear as a result of surgical ablation of their axons. This could also contribute to the reduced gain of vestibular nystagmus, OKAN and off-vertical nystagmus that was observed in some of the animals after lesion.

Animals↗
PubMed1983

Role of the flocculus and paraflocculus in optokinetic nystagmus and visual-vestibular interactions: effects of lesions.

Optokinetic nystagmus (OKN), optokinetic after-nystagmus (OKAN), vestibular nystagmus and visual-vestibular interactions were studied in monkeys after surgical ablation of the flocculus and paraflocculus. After bilateral flocculectomy the initial rapid rise in slow phase eye velocity of horizontal and vertical OKN was severely attenuated, and maximum velocities fell to the preoperative saturation level of OKAN. There is generally little or no upward OKAN in the normal monkey, and upward OKN was lost after bilateral lesions. Unilateral flocculectomy affected the rapid rise in horizontal velocity to both sides. Consistent with the absence of a rapid response to steps of surround velocity, animals were unable to follow acceleration of the visual field with eye accelerations faster than about 3-5 degrees/s2. The slow rise in OKN slow phase velocity to a steady state level was prolonged after operation. However, rates of rise were approximately equal for the same initial retinal slips before and after operation. The similarity in the time course of OKN when adjusted for initial retinal slip, and in the gain, saturation level and time course of OKAN before and after flocculectomy indicates that the lesions had not significantly altered the coupling of the visual system to the velocity storage integrator or its associated time constant. When animals were rotated in a subject-stationary visual surround after flocculectomy, they could not suppress the initial jump in eye velocity at the onset of the step. Despite this, they could readily suppress the subsequent nystagmus. The time constant of decline in the conflict situations was almost as short as in the normal monkey and was in the range of the peripheral vestibular time constant. This suggests that although the animals were unable to suppress rapid changes in eye velocity due to activation of direct vestibulo-oculomotor pathways, they had retained their ability to discharge activity from the velocity storage mechanism. Consistent with this, animals had no difficulty in suppressing OKAN after flocculectomy. Visual-vestibular interactions utilizing the velocity storage mechanism were normal after flocculectomy, as was nystagmus induced by rotation about a vertical axis or about axes tilted from the vertical. Also unaffected were the discharge of nystagmus caused by tilting the head out of the plane of the response and visual suppression of nystagmus induced by off-vertical axis rotation. The flocculus does not appear to play an important role in mediating these responses. The data before and after flocculectomy were simulated by a model which is homeomorphic to that presented previously.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1981

Visual-vestibular interaction in the flocculus of the alert monkey. I. Input activity.

Neuronal activity in the flocculus of alert Rhesus monkeys was recorded during vestibular stimulation (rotation of the monkey about a vertical axis in complete darkness), optokinetic stimulation (rotation of the visual surround around the stationary monkey), combined visual-vestibular stimulation (rotation of the monkey inside the stationary surround in light), and conflicting visual-vestibular stimulation (rotation of the monkey together with the visual surround in the same direction). The input to the flocculus was recorded as non-Purkinje cell (non-P-cell) activity. Ninety per cent of the non-P-cells which were modulated during our stimulation paradigms carry information similar to that in the neurons of vestibular nuclei. This suggests that the main mossy fiber input to the flocculus originates in the vestibular nuclei. A second input of unknown origin conveys visual information about retinal slip. Thus, part of the flocculus -- as further discussed elsewhere (Waespe and Henn 1981) -- may be specialized to subserve visual-vestibular interaction to improve the nystagmus response.

Animals↗
PubMed1981

Visual-vestibular interaction in the flocculus of the alert monkey. II. Purkinje cell activity.

The activity of Purkinje cells (P-cells) was recorded in the flocculus of alert Rhesus monkeys under different conditions of visual-vestibular stimulation. Stimulations conditions were vestibular, optokinetic, combined and conflicting. About 10--20% of all P-cells were activated in their simple spike activity during conflicting stimulation to the recording side (type I) and gave no response or much less during vestibular stimulation. About half of these P-cells were also activated during optokinetic stimulation to the recording side at velocities above 40--60 deg/s. Simple and complex spike activity behaved in a reciprocal way with overlapping but not identical working ranges. Simple spike modulation was unidirectional, complex spike activity always bidirectional. Modulation of simple spike activity cannot be related to one single parameter of the sensory input or the oculomotor output. The hypothesis is put forward that the vestibular nuclei and the flocculus behave in a complementary fashion in processing visual-vestibular information, the flocculus being specialized for high velocity optokinetic nystagmus and suppression of vestibular nystagmus.

Animals↗
PubMed1981

Vestibular nerve activity in the alert monkey during vestibular and optokinetic nystagmus.

Activity of vestibular nerve fibers and eye movements were recorded in the alert monkey during natural stimulation. The animal was rotated about a vertical axis in the dark with velocity trapezoids (vestibular), or a striped cylinder was rotated around the stationary monkey ()optokinetic), or these stimuli were combined. After velocity steps in the dark, neuronal activity declined with a dominant time constant of 5-6 s. The time constant of nystagmus recorded simultaneously was always longer, on average 23 s. Vestibular nerve activity was not influenced by optokinetic patterns or additional visual stimuli during combined visual-vestibular stimulation. Thus, in contrast to vestibular nuclei neurons, vestibular nerve activity in the alert monkey is only determined by head acceleration and cannot be related to the nystagmus response or visual stimuli.

Animals↗
PubMed1981

Input-output activity of the primate flocculus during visual-vestibular interaction.

In the primate flocculus, unit activity was recorded during vestibular (rotation of the monkey about the vertical axis in complete darkness), optokinetic (rotation of the visual surround around the stationary monkey), and conflicting (rotation of the visual surround and the turntable fixed together) stimulation. Activity indicating two different mossy fiber inputs was recorded. One carried a signal that was similar to that in the vestibular nuclei: during optokinetic stimulation, neurons saturated at a velocity of 60 degrees/second; and during conflicting stimulation, neuronal activity was attenuated only at low accelerations. This input combines vestibular, visual, and oculomotor information. Another mossy fiber input carried information about visual image slip only. This input indicates instances when nystagmus is not compensatory. Purkinje cells were modulated in their simple spike activity during optokinetic stimulation only at high stimulus velocities of 40-60 degrees/second and above, and during conflicting stimulation at high accelerations. This suggests a complementary information processing of the flocculus and the vestibular nuclei during visual-vestibular stimulation. The findings are corroborated by lesion studies in primates.

Animals↗
PubMed1980

Nystagmus slow-phase velocity during vestibular, optokinetic, and combined stimulation in the monkey.

In Rhesus monkeys the slow-phase velocity of nystagmus was measured during optokinetic, vestibular, and combined stimulation. Accelerations and decelerations of 2.5--40 degrees/s2, and rotation at constant velocities of 70-160 degrees/s were applied. During combined visual-vestibular stimulation, nystagmus slow-phase velocity is a function only of the instantaneous stimulus velocity: It has a gain near unity and is independent of the duration and value of the acceleration. The limited linear working range of the vestibular or optokinetic system is thus extended. During deceleration an inappropriate nystagmus response is elicited only when the previous constant velocity rotation was above the saturation velocity of optokinetic nystagmus (OKN). These results are related to single neuron activity recorded in the vestibular nuclei and the flocculus under identical stimulus conditions.

Acceleration↗
PubMed1980

Subjective velocity estimation during conflicting visual-vestibular stimulation.

Human subjects continuously estimated their position during and after steps of angular acceleration in complete darkness. These estimations were compared with the same vestibular stimulation in the light while subjects gazed at a striped cylinder which completely enclosed them and was mechanically fixed to the turntable. Rotation with such a fixed visual surround created a sensory conflict: the acceleration is sensed by the vestibular end organs, while the visual system senses no displacement. Accordingly, during the conflict stimulation, the estimation of rotational velocity and its duration is markedly reduced. These findings in humans compare well with nystagmus and single neuron recordings in the vestibular nuclei of alert monkeys.

Acceleration↗
PubMed1979

The velocity response of vestibular nucleus neurons during vestibular, visual, and combined angular acceleration.

In alert Rhesus monkeys neuronal activity in the vestibular nuclei was measured during horizontal angular acceleration in darkness, acceleration of an optokinetic stimulus, and combined visual-vestibular stimulation. The working ranges for visual input velocity and acceleration extend up to 60 degrees/s and 5 degrees/s2. The corresponding working range for vestibular input acceleration is wider and time-dependent. During combined stimulation, that is acceleration of the monkey in the light, a linear relation between neuronal activity and velocity could be established for all neurons. Type I vestibular plus eye movement neurons displayed the greatest sensitivity and had a small linear range of operation. Other vestibular neurons were less sensitive but had a larger range of linear response to different values of acceleration. Accelerating the animal and visual surround, simultaneously but in opposite directions, results in neuronal activity proportional to relative velocity over a limited range.

Acceleration↗
PubMed1978

Conflicting visual-vestibular stimulation and vestibular nucleus activity in alert monkeys.

In alert Rhesus monkeys (Macaca mulatta) neuronal activity of vestibular nuclei was recorded during pure vestibular and conflicting visual-vestibular stimulation. Pure vestibular stimulation consisted of rotating the monkey about the vertical axis in complete darkness. During conflicting visual-vestibular stimulation the monkeys were rotated in the light within a vertically striped cylinder mechanically coupled to the turntable. The conflict is that although the monkey is accelerated, there is no relative movement between visual surrounding and the animal. In the conflict situation thresholds of neuronal modulation and of nystagmus were raised compared with those during pure vestibular stimulation. Nystagmus slow-phase velocity could always be dissociated from the neuronal activity, the nystagmus often being totally suppressed whereas the neuronal activity was only attenuated. This suggests a further information processing between vestibular and oculomotor nuclei in the generation of nystagmus.

Animals↗
PubMed1978

Dynamic changes of optokinetic after-nystagmus (OKAN) caused by brief visual fixation periods in monkey and in man.

Optokinetic nystagmus (OKN) continues after the cessation of visual stimulation in complete darkness as primary optokinetic after-nystagmus (OKAN I). After variable periods of time, it is followed by secondary OKAN (OKAN II). Short periods of visual fixation during OKAN I in monkey and in man inhibit OKAN I, but enhance OKAN II. The enhanced OKAN II starts earlier, lasts longer, and often reaches higher slow-phase velocities than in control experiments. Therefore, OKAN II depends not on the ocurrence or strength of OKAN I, but mainly on parameters of the preceding optokinetic stimulus. Results suggest that OKAN I duration is partially determined by the development of OKAN II.

Adult↗
PubMed1978

Reciprocal changes in primary and secondary optokinetic after-nystagmus (OKAN) produced by repetitive optokinetic stimulation in the monkey.

In six rhesus monkeys (Macaca mulatta) the effect of repetitive periods of whole-field optokinetic stimulation upon the different phases of optokinetic after-nystagmus (OKAN) was studied. The precedings optokinetic stimulus consisted of rotating a striped cylinder around the stationary monkey. Experiments were performed on up to 8 successive days. The results demonstrate that OKAN I and OKAN II are affected in a reverse manner by repeated optokinetic stimulation: The duration of OKAN I strongly decreases, whereas OKAN II increases in duration and intensity. The mechanisms under lying the generation of OKAN I and OKAN II and the role of OKAN II in the habituation process are discussed.

Animals↗
PubMed1977

Vestibular nuclei activity during optokinetic after-nystagmus (OKAN) in the alert monkey.

Neurons which receive an input from the horizontal semicircular canals were recorded from the vestibular nuclei in chronically prepared monkeys (Macaca mulatta) during optokinetic after-nystagmus (OKAN). In complete darkness the vestibular neurons showed activity changes which closely paralleled the strength of nystagmus. The activity of vestibular units returned to baseline levels of spontaneous discharge only when all after-nystagmus had ceased, or when it was inhibited by stationary visual stimuli. The possible role of vestibular neurons in the generation of OKAN and its significance in vestibulo-visual interaction is discussed.

Animals↗
PubMed1977

Neuronal activity in the vestibular nuclei of the alert monkey during vestibular and optokinetic stimulation.

Recordings from neurons of the vestibular nuclei were performed in alert monkeys. Type I and type II units were identified by rotating the monkey about a vertical axis. Al neurons responded also when only the visual surround was rotated around the stationary monkey. The combination of visual and vestibular stimulation points towards non-algebraic summation characteristics for the two inputs, with each input dominating the response over a certain range.

Animals↗
PubMed1976

Duration and direction of optokinetic after-nystagmus as a function of stimulus exposure time in the monkey.

1. Parameters of the optokinetic after-nystagmus (OKAN) outlasting optokinetic stimulation were studied in monkeys. With constant pattern velocity (60 degrees/s) exposure times were varied between 2 s and 15 min. 2. All monkeys showed a primary after-nystagmus moving in the same direction (OKAN I) as the preceding optokinetic nystagmus, under all conditions tested. A secondary after-nystagmus in the opposite direction (OKAN II), was only observed after exposure times of 30 s or longer. After a 15-min exposure, half of the monkeys showed an early onset of OKAN II in less than 1 min, whereas for the remaining half the transition to OKAN II occurred only after 4 min or not at all. 3. In monkeys showing an early onset of OKAN II, the duration of OKAN I decreased and the maximal slow phase velocity of OKAN II increased consistently with longer exposure times. In several instances OKAN III, moving in the same direction as OKAN I, was seen after OKAN II. 4. Monkeys in which OKAN II was late, or absent, often showed minima and additional maxima of slow phase velocity of OKAN. 5. The results are discussed in terms of two opposing mechanisms underlying the generation of OKAN and their connections to the vestibular system.

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