Differential Effects of Reflex Blinks on Saccade Perturbations in Humans

2010 ◽  
Vol 103 (3) ◽  
pp. 1685-1695 ◽  
Author(s):  
H.H.L.M. Goossens ◽  
A. J. Van Opstal

Studies in both humans and monkeys have indicated that blinks affect the central programming of saccades. In this study, we compared the influence of two types of reflex blinks on the trajectories and kinematics of memory-guided saccades in human subjects. We found that electrical stimulation of the supraorbital nerve shortly before or during a saccade briefly halts or decelerates the eye in midflight. After this short interruption, the eye always resumed its course and reached the target location in the absence of visual feedback. Air puff stimuli produced significant decreases in mean eye velocity too, but in addition to these changes in saccade kinematics, they produced much larger and more variable perturbations of the two-dimensional saccade trajectories. Even so, the endpoints of blink-perturbed saccades obtained under both test conditions remained as accurate and as precise as those observed in the control condition. We hypothesize that the reduction in mean eye velocity is not caused by a trigeminal reactivation of brain stem omnipause neurons but could instead arise from a trigeminal transient inhibition of saccade-related activity in the midbrain superior colliculus (SC). These findings support the theory that blink-perturbed saccades are programmed as slow, but straight, saccades onto which blink-related eye movements are superimposed. This linear superposition occurs downstream from the SC.

1992 ◽  
Vol 68 (6) ◽  
pp. 1967-1985 ◽  
Author(s):  
M. A. Segraves

1. This study identified neurons in the rhesus monkey's frontal eye field that projected to oculomotor regions of the pons and characterized the signals sent by these neurons from frontal eye field to pons. 2. In two behaving rhesus monkeys, frontal eye field neurons projecting to the pons were identified via antidromic excitation by a stimulating microelectrode whose tip was centered in or near the omnipause region of the pontine raphe. This stimulation site corresponded to the nucleus raphe interpositus (RIP). In addition, electrical stimulation of the frontal eye field was used to demonstrate the effects of frontal eye field input on neurons in the omnipause region and surrounding paramedian pontine reticular formation (PPRF). 3. Twenty-five corticopontine neurons were identified and characterized. Most frontal eye field neurons projecting to the pons were either movement neurons, firing in association with saccadic eye movements (48%), or foveal neurons responsive to visual stimulation of the fovea combined with activity related to fixation (28%). Corticopontine movement neurons fired before, during, and after saccades made within a restricted movement field. 4. The activity of identified corticopontine neurons was very similar to the activity of neurons antidromically excited from the superior colliculus where 59% had movement related activity, and 22% had foveal and fixation related activity. 5. High-intensity, short-duration electrical stimulation of the frontal eye field caused omnipause neurons to stop firing. The cessation in firing appeared to be immediate, within < or = 5 ms. The time that the omnipause neuron remained quiet depended on the intensity of the cortical stimulus and lasted up to 30 ms after a train of three stimulus pulses lasting a total of 6 ms at an intensity of 1,000 microA. Low-intensity, longer duration electrical stimuli (24 pulses, 75 microA, 70 ms) traditionally used to evoke saccades from the frontal eye field were also followed by a cessation in omnipause neuron firing, but only after a delay of approximately 30 ms. For these stimuli, the omnipause neuron resumed firing when the stimulus was turned off. 6. The same stimuli that caused omnipause neurons to stop firing excited burst neurons in the PPRF. The latency to excitation ranged from 4.2 to 9.8 ms, suggesting that there is at least one additional neuron between frontal eye field neurons and burst neurons in the PPRF. 7. The present study confirms and extends the results of previous work, with the use of retrograde and anterograde tracers, demonstrating direct projections from the frontal eye field to the pons.(ABSTRACT TRUNCATED AT 400 WORDS)


2015 ◽  
Vol 113 (10) ◽  
pp. 3866-3892 ◽  
Author(s):  
James O. Phillips ◽  
Leo Ling ◽  
Kaibao Nie ◽  
Elyse Jameyson ◽  
Christopher M. Phillips ◽  
...  

Animal experiments and limited data in humans suggest that electrical stimulation of the vestibular end organs could be used to treat loss of vestibular function. In this paper we demonstrate that canal-specific two-dimensionally (2D) measured eye velocities are elicited from intermittent brief 2 s biphasic pulse electrical stimulation in four human subjects implanted with a vestibular prosthesis. The 2D measured direction of the slow phase eye movements changed with the canal stimulated. Increasing pulse current over a 0–400 μA range typically produced a monotonic increase in slow phase eye velocity. The responses decremented or in some cases fluctuated over time in most implanted canals but could be partially restored by changing the return path of the stimulation current. Implantation of the device in Meniere's patients produced hearing and vestibular loss in the implanted ear. Electrical stimulation was well tolerated, producing no sensation of pain, nausea, or auditory percept with stimulation that elicited robust eye movements. There were changes in slow phase eye velocity with current and over time, and changes in electrically evoked compound action potentials produced by stimulation and recorded with the implanted device. Perceived rotation in subjects was consistent with the slow phase eye movements in direction and scaled with stimulation current in magnitude. These results suggest that electrical stimulation of the vestibular end organ in human subjects provided controlled vestibular inputs over time, but in Meniere's patients this apparently came at the cost of hearing and vestibular function in the implanted ear.


2016 ◽  
Vol 115 (3) ◽  
pp. 1132-1145 ◽  
Author(s):  
Laurence C. Jayet Bray ◽  
Sonia Bansal ◽  
Wilsaan M. Joiner

Extraretinal information, such as corollary discharge (CD), is hypothesized to help compensate for saccade-induced visual input disruptions. However, support for this hypothesis is largely for one-dimensional transsaccadic visual changes, with little comprehensive information on the spatial characteristics. Here we systematically mapped the two-dimensional extent of this compensation by quantifying the insensitivity to different displacement metrics. Human subjects made saccades to targets positioned at different amplitudes (4° or 8°) and directions (rightward, oblique, or upward). After the saccade the initial target disappeared and, after a blank period, reappeared at a shifted location—a collinear, diagonal, or orthogonal displacement. Subjects reported the perceived shift direction, and we determined the displacement detection based on the perceptual judgments. The two-dimensional insensitivity fields resulting from the perceptual thresholds had spatial features similar to the saccadic eye movement variability: 1) scaled with movement amplitude, 2) oriented (less sensitive to the change) along the saccade vector, and 3) approximately constant in shape when normalized by movement amplitude. In addition, comparing the postsaccadic perceptual estimate of the presaccadic target location to that based solely on the postsaccade visual error showed that overall the perceptual estimate was approximately 50% more accurate and 35% less variable than estimates based solely on this visual information. However, this relationship was not uniform: The benefit of extraretinal information was observed largely for displacements with a component parallel to the saccade vector. These results suggest a graded use of extraretinal information when forming the postsaccadic perceptual evaluation of transsaccadic environmental changes.


2000 ◽  
Vol 83 (4) ◽  
pp. 2443-2452 ◽  
Author(s):  
Simo Vanni ◽  
Kimmo Uutela

When attending to a visual object, peripheral stimuli must be monitored for appropriate redirection of attention and gaze. Earlier work has revealed precentral and posterior parietal activation when attention has been directed to peripheral vision. We wanted to find out whether similar cortical areas are active when stimuli are presented in nonattended regions of the visual field. The timing and distribution of neuromagnetic responses to a peripheral luminance stimulus were studied in human subjects with and without attention to fixation. Cortical current distribution was analyzed with a minimum L1-norm estimate. Attention enhanced responses 100–160 ms after the stimulus onset in the right precentral cortex, close to the known location of the right frontal eye field. In subjects whose right precentral region was not distinctly active before 160 ms, focused attention commonly enhanced right inferior parietal responses between 180 and 240 ms, whereas in the subjects with clear earlier precentral response no parietal enhancement was detected. In control studies both attended and nonattended stimuli in the peripheral visual field evoked the right precentral response, whereas during auditory attention the visual stimuli failed to evoke such response. These results show that during focused visual attention the right precentral cortex is sensitive to stimuli in all parts of the visual field. A rapid response suggests bypassing of elaborate analysis of stimulus features, possibly to encode target location for a saccade or redirection of attention. In addition, load for frontal and parietal nodi of the attentional network seem to vary between individuals.


1999 ◽  
Vol 82 (3) ◽  
pp. 1198-1208 ◽  
Author(s):  
Kaoru Yoshida ◽  
Yoshiki Iwamoto ◽  
Sohei Chimoto ◽  
Hiroshi Shimazu

Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events in OPNs and thereby determine what patterns of afferent discharge impinge on OPNs to cause their saccadic inhibition. The membrane potential of impaled OPNs exhibited steep hyperpolarization before each saccade that lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of Cl− ions, indicating it consisted of temporal summation of inhibitory postsynaptic potentials (IPSPs). The duration of the saccade-related hyperpolarization was almost equal to the duration of the concurrent saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was correlated significantly with the peak eye velocity. The time integral of the hyperpolarization was correlated with the radial amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time (∼20 ms) of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The initial steep hyperpolarization led the beginning of saccades by 15.9 ± 3.8 (SD) ms, which is longer than the lead time for medium-lead burst neurons. These results demonstrate that the pause of activity in OPNs is caused by IPSPs initiated by an abrupt, intense input and maintained, for the whole duration of the saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and frontal eye fields and that the eye velocity-related inhibition originates from the burst generator in the brain stem.


2021 ◽  
Author(s):  
Hongchao Xie ◽  
Xiangpeng Luo ◽  
Gaihua Ye ◽  
Zhipeng Ye ◽  
Haiwen Ge ◽  
...  

Abstract Twist engineering, or the alignment of two-dimensional (2D) crystalline layers with desired orientations, has led to tremendous success in modulating the charge degree of freedom in hetero- and homo-structures, in particular, in achieving novel correlated and topological electronic phases in moiré electronic crystals. However, although pioneering theoretical efforts have predicted nontrivial magnetism and magnons out of twisting 2D magnets, experimental realization of twist engineering spin degree of freedom remains elusive. Here, we leverage the archetypal 2D Ising magnet chromium triiodide (CrI3) to fabricate twisted double bilayer homostructures with tunable twist angles and demonstrate the successful twist engineering of 2D magnetism in them. Using linear and circular polarization-resolved Raman spectroscopy, we identify magneto-Raman signatures of a new magnetic ground state that is sharply distinct from those in natural bilayer (2L) and four-layer (4L) CrI3. With careful magnetic field and twist angle dependence, we reveal that, for a very small twist angle (~ 0.5 degree), this emergent magnetism can be well-approximated by a weighted linear superposition of those of 2L and 4L CI3 whereas, for a relatively large twist angle (~ 5 degree), it mostly resembles that of isolated 2L CrI3. Remarkably, at an intermediate twist angle (~ 1.1 degree), its magnetism cannot be simply inferred from the 2L and 4L cases, because it lacks sharp spin-flip transitions that are present in 2L and 4L CrI3 and features a dramatic Raman circular dichroism that is absent in natural 2L and 4L ones. Our results demonstrate the possibility of designing and controlling the spin degree of freedom in 2D magnets using twist engineering.


1985 ◽  
Vol 116 (1) ◽  
pp. 1-25 ◽  
Author(s):  
P. A. Kerfoot ◽  
G. O. Mackie ◽  
R. W. Meech ◽  
A. Roberts ◽  
C. L. Singla

In the jellyfish Aglantha digitale escape swimming is mediated by the nearly synchronous activity of eight giant motor axons which make direct synaptic contact with contractile myoepithelial cells on the under-surface of the body wall. The delay in transmission at these synapses was 0.7 +/− 0.1 ms (+/− S.D.;N = 6) at 12 degrees C as measured from intracellular records. Transmission depended on the presence of Ca2+ in the bathing medium. It was not blocked by increasing the level of Mg2+ to 127 mmol l-1. The myoepithelium is a thin sheet of electrically coupled cells and injection of current at one point was found to depolarize the surrounding cells. The potential change declined with distance from the current source as expected for two-dimensional current spread. The two-dimensional space constant (lambda) was 770 micron for current flow in the circular direction and 177 micron for radial flow. The internal resistance of the epithelium (178–201 omega cm) and the membrane time constant (5–10 ms) were direction independent. No propagated epithelial action potentials were observed. Spontaneous miniature synaptic potentials of similar amplitude and rise-time were recorded intracellularly at distances of up to 1 mm from the motor giant axon. Ultrastructural evidence confirms that neuro-myoepithelial synapses also occur away from the giant axons. It is likely that synaptic sites are widespread in the myoepithelium, probably associated with the lateral motor neurones as well as the giant axons. Local stimulation of lateral motor neurones generally produced contraction in distinct fields. We suppose that stimulation of a single motor giant axon excites a whole population of lateral motor neurones and hence a broad area of the myoepithelium.


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