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PubMedDate not supplied

Effect of incisions in the brainstem commissural network on the short-term vestibulo-ocular adaptation of the cat.

This study was intended to test the adaptive plasticity of the vestibulo-ocular reflex before and after either a midsagittal or parasagittal incision in the brainstem. Eye movements were measured with the electromagnetic search coil technique during the vestibulo-ocular reflex (VORD) in the dark, the optokinetic reflex (OKN), and the visuo-vestibular adaptive training procedure. Two types of visual-vestibular combined stimulation were applied by means of low frequency stimuli (0.05 to 0.10 Hz). In order to increase or decrease the VORD gain, the optokinetic drum was oscillated either 180 degrees out-of-phase or in-phase with the vestibular stimulus turntable. This "training" procedure was applied for 4 hours. Initial measurements of the VORD were normal with a mean gain value of 0.92 +/- 0.08. After 4 hours of "training" with the out-of-phase condition (180 degrees), VORD gain reached mean values of 1.33 +/- 0.11 (n = 6 cats). In the in-phase combination, the mean VORD gain decreased from 1.0 to 0.63 +/- 0.02 (n = 2 cats). No significant change of VORD phase was found in any of the cats. Midsagittal or parasagittal pontomedullary brainstem incisions were performed in 4 cats. Recovery of the VOR was tested on the 2nd, 7th, and 30th day after operation. After the 30th day, recovery of the VORD gain stabilized at about 66% of the initial preoperative value. At this stage of the recovery, the optokinetic response (OKN) of the midsagittal-lesioned cats was practically normal: in the parasagittal-lesioned cats, the postoperative OKN responses were asymmetric. After stabilization of recovery, lesioned cats were trained with the same adaptation procedure. Although the direct effect of the visuo-vestibular combined stimulation during the training was still operative in all lesioned cats, the adaptive plasticity was completely abolished by the lesions. These results suggest that the commissural brainstem network may play a crucial role in the acquisition of the forced VOR adaptation.

Adaptation, Ocular↗
PubMed1998

Short-term vestibulo-ocular adaptation: influence of context.

A number of mechanisms and strategies are used to help an individual compensate for loss of labyrinthine function. One important example is the ability to produce a preplanned motor response that anticipates the motion of the head and so compensates for it. Closely tied to this phenomenon is the gating, in or out, of a learned response on the basis of the context in which it must occur. This issue is particularly relevant to designing programs of physical therapy that optimize performance for natural behavior. Here we discuss a model of short-term vestibulo-ocular adaptation-adjustment of vestibulo-ocular phase (timing)-and how it can be used to study context-dependent vestibulo-ocular learning. We will show how vestibulo-ocular phase can be adjusted by selectively altering the common velocity-to-position ocular motor neural integrator for one type of eye movement (vestibular) and not for another (saccades), or for one type of head movement (sinusoidal) and not for another (step). These results are another example of the remarkable flexibility of the vestibulo-ocular adaptive mechanism and further show that the fundamental process of integration for eye movements can be modified according to the pattern of afferent information.

Adaptation, Physiological↗
PubMed1976

Extreme vestibulo-ocular adaptation induced by prolonged optical reversal of vision.

1. These experiments investigated plastic changes in the vestibulo-ocular reflex (VOR) of human subjects consequent to long-term optical reversal of vision during free head movement. Horizontal vision-reversal was produced by head-mounted dove prisms. Four normal adults were continuously exposed to these conditions during 2, 6, 7 and 27 days respectively.2. A sinusoidal rotational stimulus, previously shown to be nonhabituating (1/6 Hz; 60 degrees /sec amplitude), was used to test the VOR in the dark at frequent intervals both during the period of vision-reversal and an equal period after return to normal vision. D.c. electro-oculography (EOG) was used to record eye movement, taking care to avoid changes of EOG gain due to light/dark adaptation of the retina.3. All subjects showed substantial reduction of VOR gain (eye velocity/head velocity) during the first 2 days of vision-reversal. The 6-, 7- and 27-day subjects showed further reduction of gain which reached a low plateau at about 25% the normal value by the end of one week. At this time the attenuation of some EOG records was so marked as to defy extraction of a meaningful sinusoidal signal.4. After removal of the prisms VOR gain recovered along a time course which approximated that of the original adaptive attenuation.5. In the 27-day experiment large changes of phase developed in the VOR during the second week of vision-reversal. These changes generally progressed in a lagging sense, to reach 130 degrees phase lag relative to normal by the beginning of the third week. Accompanying this was a considerable restoration of gain from 25 to 50% the normal value. These adapted conditions, which approximate functional reversal of the reflex, were then maintained steady, even overnight, until return to normal vision on the 28th day.6. Thereafter, whereas VOR phase returned to near-normal in 2 hr, restoration of gain occupied a further 2-3 weeks.7. There was a highly systematic relation between instantaneous gain and phase, even during periods of widely fluctuating change associated with transition from one steady state to another. During such transition there was a tendency for directional preponderance to occur in the VOR.8. All the observed changes were highly specific to the plane of vision-reversal, no VOR changes being observed in the sagittal plane.9. VOR changes were adaptive, in the sense that they were always goal-directed towards the requirements of retinal image stabilization during head movement. They were plastic to the extent that there was extensive and retained remodelling of the reflex towards this goal.10. It is inferred that all the observed changes in gain and phase are compatible with a simple neural network employing known vestibulo-ocular projections via brainstem and cerebellar pathways, providing that the reversed visual tracking task can produce plastic modulation of efficacy in the cerebellar pathway and that this pathway exhibits a dynamic characteristic producing moderate phase lead in a sinusoidal signal at 1/6 Hz.

Journal Article↗
PubMed2006

Simulated annealing in ocular adaptive optics.

We present what is to our knowledge a first hardware realization of a simulated annealing algorithm in an adaptive optics system designed to image the retina of the human eye. The algorithm is applied to the retinal image itself without the need for wavefront sensors in the system. We find that this optimization algorithm can be an alternative to the traditional Hartmann-Shack sensing. We also compare the simulated annealing algorithm to the stochastic parallel gradient descent algorithm.

Algorithms↗
PubMed1995

Cerebellar nitric oxide is necessary for vestibulo-ocular reflex adaptation, a sensorimotor model of learning.

1. Nitric oxide (NO) production in the nervous system has been implicated in cellular mechanisms of learning and memory. Our study investigates an in vivo sensorimotor model of learning. It demonstrates that a localized vestibulocerebellar injection of the NO synthase inhibitor, L-NG-monomethyl-arginine (L-NMMA), which specifically blocks NO production, inhibited the acquisition of adaptive vestibulo-ocular reflex (VOR) gain increases but not gain decreases in the goldfish. 2. Restoration of NO production by concomitant administration of L-arginine (the substrate for NO synthase) and L-NMMA suppressed the inhibitory effect of L-NMMA on adaptive gain increases. 3. This effect of L-NMMA was stereospecific because injection of D-NMMA did not suppress adaptive VOR gain increases. 4. Injection of L-NMMA after VOR adaptation had no effect on retention, failing to alter the postadaptive recovery after a VOR gain increase. 5. In conclusion, acquisition of adaptive VOR gain increases are affected by cerebellar NO inhibition. However, because gain decreases are not, they may involve either non-NO cerebellar or extracerebellar mechanisms. In addition, different processes for acquisition and retention of gain increases may be operating, because inhibition of cerebellar NO affects the acquisition but not the retention phase.

Adaptation, Ocular↗