Search

Background Acute acquired concomitant esotropia (AACE) is an unusual presentation characterized by acute onset of esotropia after infancy. For patients with AACE of adulthood, the outcome of surgery, which is a common treatment, often shows successful recovery of stereopsis. However, whether surgically corrected patients with AACE of adulthood achieved balanced eyes is yet unclear. Methods Here, we used a binocular phase combination paradigm to quantitatively assess the ocular dominance of 22 surgically aligned patients with AACE of adulthood, which all had regained normal stereopsis after the surgery and 14 adult controls with normal vision. The sensory eye dominance was quantified as the interocular contrast ratio, termed balance point, at which each eye contributed equally to the perception of cyclopean grating. Results We found that, normal controls had a mean balance point value close to unity (0.96 ± 0.01), whereas adult AACE patients exhibited apparent interocular imbalance (0.76 ± 0.04), which was significantly different from control group (Mann–Whitney U = 135, P < 0.001, two tailed). In addition, the balance point of adults with AACE didn't correlate with the interval between onset of esotropia and the surgery (r = − 0.262, p = 0.239), or the length of postoperative follow-up period (r = 0.127, p = 0.575). Conclusion Our results suggest that, for patients with AACE of adulthood whose eyes had been straightened, there is still residual sensory imbalance which may be a potential risk factor for AACE of adulthood.

Volitional motivation is quantitatively evaluated by the M1 neural activity in response to progressively escalating volitional efforts. Striatopallidal pathway and adenosine ATask-dependent volitional control of the selected neural activity in the cortex is critical to neuroprosthetic learning to achieve reliable and robust control of the external device. The volitional control of neural activity is driven by a motivational factor (volitional motivation), which directly reinforces the target neurons via real-time biofeedback. But in the absence of motor behavior, how to evaluate the volitional motivation? Here, we defined the criterion (△F/F) of calcium fluorescence signal in volitionally controlled neural task, then escalated the efforts by progressively increasing the number of times for reaching the criterion or holding time after reaching the criterion. We devised the calcium-based progressive threshold-crossing events (termed "Calcium PTE") and calcium-based progressive threshold-crossing holding-time (termed "Calcium PTH") for quantitative assessment of volitional motivation in respond to progressively escalating efforts. Furthermore, we used this novel neural representation of the volitional motivation to explore the neural circuit and neuromodulator bases for volitional motivation. Like behavioral motivation, chemogenetic activation and pharmacological blockade of the striatopallidal pathway decreased and increased, respectively, the breakpoints of the "Calcium PTE" and "Calcium PTH" responding to escalating efforts. Furthermore, volitional and behavioral motivation shared similar dopamine dynamics in the nucleus accumbens in response to trial-by-trial escalating efforts. In general, the development of neural representation of volitional motivation may open new avenue for smooth and effective control of BMI task. Abstract figure legend Evaluation scheme of volitional motivation and behavioral motivation This article is protected by copyright. All rights reserved.

The cost-benefit decision-making (CBDM) is critical to normal human activity and a diminished willingness to expend effort to obtain rewards is a prevalent/noted characteristic of neuropsychiatric disorders such as schizophrenia, Parkinson's disease. Numerous studies have identified nucleus accumbens (NAc) as an important locus for CBDM control but their neuromodulatory and behavioral mechanisms remain largely under-explored. Adenosine A

Human visual function degrades with age. Previous studies of visual perception have shown that aged people have worse performance in the coding of orientation information. However, the neuronal mechanism still remains elusive. In this study, we performed in vivo extracellular single-unit recording in the primary visual cortex of senescent and young monkeys, and we used the Chernoff distance to quantify the encoded information of neurons for fine and coarse orientation difference. Our results showed that the Chernoff distance for fine orientation difference in senescent monkeys is significantly smaller than that in young monkeys. In contrast, the Chernoff distance for the coarse coding was comparable in young and old groups. Meanwhile, increased spontaneous response and maximum evoked response was also observed. Further investigation of neuronal correlation showed higher noise and signal correlations in aging monkeys than that in young monkeys. These correlation changes predicted a detrimental effect on the efficiency of population coding of orientation information. Taken together, our results suggest that the information coding efficiency of orientation information is impaired during aging and might account for the degradation of performance in human fine orientation discrimination task.

Purpose We developed a stereo task that is based on a motion direction discrimination to examine the role that depth can play in disambiguating motion direction. Methods In this study, we quantified normal adults’ static and dynamic (i.e., laterally moving) stereoscopic performance using a psychophysical task, where we dichoptically presented randomly arranged, limited lifetime Gabor elements at two depth planes (one plane was at the fixation plane and the other at an uncrossed disparity relative to the fixation plane). Each plane contained half of the elements. For the dynamic condition, all elements were vertically oriented and moved to the left in one plane and to the right in another plane; for the static condition, the elements were horizontally oriented in one plane and vertically oriented in another plane. Results For the range of motion speed that we measured (from 0.17°/s to 5.33°/s), we observed clear speed tuning of the stereo sensitivity (P = 3.0 × 10−5). The shape of this tuning did not significantly change with different spatial frequencies. We also found a significant difference in stereo sensitivity between stereopsis with static and laterally moving stimuli (speed = 0.67°/s; P = 0.004). Such difference was not evident when we matched the task between the static and moving stimuli. Conclusions We report that lateral motion modulates human global depth perception. This motion/stereo constraint is related to motion velocity not stimulus temporal frequency. We speculate that the processing of motion-based stereopsis of the kind reported here occurs in dorsal extrastriate cortex.

Background: Adults with late-onset acute acquired concomitant esotropia (AACE) have chance to develop normal binocular functions including a balanced ocular dominance before the onset of esotropia. For most patients, strabismus surgery re-establishing the ocular alignment indeed effectively restore stereopsis and visual acuity to the normal level. However, it is unclear whether they have already acquired balanced two eyes.Methods: 11 surgically aligned patients with AACE (24.3 ± 1.5 years; mean ± SE) and 14 adults with normal vision (26.1±1.2 years) participated in our experiments. All patients had normal binocularity and stereopsis. Using binocular phase combination paradigm, sensory eye dominance was quantified as the interocular contrast ratio, termed balance point, at which the contribution of each eye to the perception of cyclopean grating were equal.Results: Normal controls had a mean balance point value close to unity (0.95±0.01), while AACE group exhibited evident binocular imbalance (0.76±0.05), which was significantly different from control group (t (10.45) = -3.485, p = 0.006) . The balance point value didn’t depend on the interval from AACE onset to strabismus surgery (r = -0.357, p = 0.281) or the interval from the surgery to examination of sensory eye dominance (r = -0.105, p = 0.759).Conclusions: Although strabismus surgery effectively straightened AACE patients’ ocular alignment and even conferred them normal stereopsis, late-onset AACE patients’ two eyes were still not balanced. These results indicated that binocular imbalance might be a risk factor for adult AACE.

Volitional control is at the core of brain-machine interfaces (BMI) adaptation and neuroprosthetic-driven learning to restore motor function for disabled patients, but neuroplasticity changes and neuromodulation underlying volitional control of neuroprosthetic learning are largely unexplored. To better study volitional control at annotated neural population, we have developed an operant neuroprosthetic task with closed-loop feedback system by volitional conditioning of population calcium signal in the M1 cortex using fiber photometry recording. Importantly, volitional conditioning of the population calcium signal in M1 neurons did not improve within-session adaptation, but specifically enhanced across-session neuroprosthetic skill learning with reduced time-to-target and the time to complete 50 successful trials. With brain-behavior causality of the neuroprosthetic paradigm, we revealed that proficiency of neuroprosthetic learning by volitional conditioning of calcium signal was associated with the stable representational (plasticity) mapping in M1 neurons with the reduced calcium peak. Furthermore, pharmacological blockade of adenosine A

Recently, it has been shown that short-term monocular deprivation in adult humans can temporally shift the ocular dominance in favor of the deprived eye. It is not clear whether this form of ocular dominance plasticity can be explained by cortical contrast adaptation, which is known to be orientationally selective. Here we show that if only one eye is deprived of a limited band of orientations for a short period of 2.5 h, the deprived eye’s contribution to binocular function at all orientations rather than just those corresponding to the previously deprived orientations is strengthened. This isotropic enhancement is quite different from the orientational enhancement previously reported and suggests a separate neuroplastic mechanism specific to binocular function.

How to precisely quantify the binocular eye balance (i.e., the contribution that each eye makes to the binocular percept) across a range of spatial frequencies using a binocular combination task, is an important issue in both clinical and basic research. In this study, we aimed to compare the precision of a binocular orientation combination paradigm with that of the standard binocular phase combination paradigm in measuring the binocular eye balance at low to high spatial frequencies. Nine normal adults (average age: 24.6 ± 2.0 years old) participated. Subjects viewed an LED screen dichoptically with polarized glasses in a dark room. The method of constant stimuli was used to quantitatively assess the point of subjective equality (PSE), i.e., the interocular contrast ratio when two eyes are balanced in binocular combination, for stimulus spatial frequencies from 0.5 to 8 cycles/degree. Precision was quantified by the variance [i.e., standard error (SE), obtained from 100 bootstrap estimates] associated to the PSE. Using stimuli whose interocular phase difference at the edge of the gratings was matched at 45°, we found that the orientation paradigm provides more precision than the standard binocular phase combination paradigm, especially at high frequencies (Experiment 1). Such differences remained when using stimuli that had three times larger interocular phase difference (Experiment 2) or displayed at four times higher stimuli resolution (Experiment 3). Our results indicate that a binocular combination tasked based on orientation rather than phase, provides a more precise estimate of binocular eye balance in human adults at high spatial frequencies, thus allowing a binocular balance to be assessed within the spatial region where amblyopes are most defective (i.e., high spatial frequencies).

Volitional control is at the core of brain-machine interfaces (BMI) adaptation and neuroprosthetic-driven learning to restore motor function for disabled patients, but neuroplasticity changes and neuromodulation underlying volitional control of neuroprosthetic learning are largely unexplored. To better study volitional control at annotated neural population, we have developed an operant neuroprosthetic task with closed-loop feedback system by volitional conditioning of population calcium signal in the M1 cortex using fiber photometry recording. Importantly, volitional conditioning of the population calcium signal in M1 neurons did not improve within-session adaptation, but specifically enhanced across-session neuroprosthetic skill learning with reduced time-to-target and the time to complete 50 successful trials. With brain-behavior causality of the neuroprosthetic paradigm, we revealed that proficiency of neuroprosthetic learning by volitional conditioning of calcium signal was associated with the stable representational (plasticity) mapping in M1 neurons with the reduced calcium peak. Furthermore, pharmacological blockade of adenosine A2A receptors facilitated volitional conditioning of neuroprosthetic learning and converted an ineffective volitional conditioning protocol to be the effective for neuroprosthetic learning. These findings may help to harness neuroplasticity for better volitional control of neuroprosthetic training and suggest a novel pharmacological strategy to improve neuroprosthetic learning in BMI adaptation by targeting striatal A2A receptors.

Action video gaming can promote neural plasticity. Short-term monocular patching drives neural plasticity in the visual system of human adults. For instance, short-term monocular patching of 0.5–5 h briefly enhances the patched eye’s contribution in binocular vision (i.e., short-term ocular dominance plasticity). In this study, we investigate whether action video gaming can influence this plasticity in adults with normal vision. We measured participants’ eye dominance using a binocular phase combination task before and after 2.5 h of monocular patching. Participants were asked to play action video games, watch action video game movies, or play non-action video games during the period of monocular patching. We found that participants’ change of ocular dominance after monocular patching was not significantly different either for playing action video games versus watching action video game movies (Comparison 1) or for playing action video games versus playing non-action video games (Comparison 2). These results suggest that action video gaming does not either boost or eliminate short-term ocular dominance plasticity, and that the neural site for this type of plasticity might be in the early visual pathway.

If one eye is patched for a period of 2.5 h in human adults, transient changes in sensory eye dominance result with the previously patched eye’s contribution being strengthened. Similar changes result from opaque and translucent occlusion suggesting that it is the deprivation of contrast not luminance information that drives these transient shift of sensory eye dominance. However, this does not rule out the possibility that luminance deprivation per se cannot produce changes in sensory eye dominance, indeed based on what we know of the physiology, where the contrast gain of visual neurons is luminance dependent, one would expect it should. We show that if the mean luminance of one eye is reduced 1000-fold for a period of 2.5 h, there are subsequent changes in sensory eye dominance. With further control experiments we show that this deprivation effect critically depends on the absolute luminance of each eye rather than the relative interocular luminance imbalance. These results indicate that changes in contrast gain at an early, monocular stage of the pathway can result in the transient shift of sensory eye dominance.

Scientific Reports 6: Article number: 24769; published online: 20 April 2016; updated: 10 February 2017. The Acknowledgements section in this Article is incomplete: ‘The authors thank Dr. Jiabo Tan, Mr. Shuya Han for valuable help in behavioral experiments. This work was supported by the National Natural Science Foundation of China (NSFC 81261120562 to YZ and NSFC 81500754 to JZ) and the Canadian Institutes of Health Research Grants (MOP-53346, CCI-125686 & MT-10818 to RFH).

It is well known that, in humans, contrast sensitivity training at high spatial frequency (SF) not only leads to contrast sensitivity improvement, but also results in an improvement in visual acuity as assessed with gratings (direct effect) or letters (transfer effect). However, the underlying neural mechanisms of this high spatial frequency training improvement remain to be elucidated. In the present study, we examined four properties of neurons in primary visual cortex (area 17) of adult cats that exhibited significantly improved acuity after contrast sensitivity training with a high spatial frequency grating and those of untrained control cats. We found no difference in neuronal contrast sensitivity or tuning width (Width) between the trained and untrained cats. However, the trained cats showed a displacement of the cells’ optimal spatial frequency (OSF) to higher spatial frequencies as well as a larger neuronal signal-to-noise ratio (SNR). Furthermore, both the neuronal differences in OSF and SNR were significantly correlated with the improvement of acuity measured behaviorally. These results suggest that striate neurons might mediate the perceptual learning-induced improvement for high spatial frequency stimuli by an alteration in their spatial frequency representation and by an increased SNR.

A fundamental task of the visual system is to extract figure–ground boundaries between images of objects, which in natural scenes are often defined not only by luminance differences but also by “second-order” contrast or texture differences. Responses to contrast modulation (CM) and other second-order stimuli have been extensively studied in human psychophysics, but the neuronal substrates of second-order responses in nonhuman primates remain poorly understood. In this study, we have recorded single neurons in area V2 of macaque monkeys, using both CM patterns as well as conventional luminance modulation (LM) gratings. CM stimuli were constructed from stationary sine wave grating carrier patterns, which were modulated by drifting envelope gratings of a lower spatial frequency. We found approximately one-third of visually responsive V2 neurons responded to CM stimuli with a pronounced selectivity to carrier spatial frequencies, and often orientations, that were clearly outside the neurons' passbands for LM gratings. These neurons were “form-cue invariant” in that their tuning to CM envelope spatial frequency and orientation was very similar to that for LM gratings. Neurons were tuned to carrier spatial frequencies that were typically 2–4 octaves higher than their optimal envelope spatial frequencies, similar to results from human psychophysics. These results are distinct from CM responses arising from surround suppression, but could be understood in terms of a filter-rectify-filter model. Such neurons could provide a functionally useful and explicit representation of segmentation boundaries as well as a plausible neural substrate for human perception of second-order boundaries.

It is well known that, in humans, contrast sensitivity training at high spatial frequency (SF) not only leads to contrast sensitivity improvement, but also results in an improvement in visual acuity as assessed with gratings (direct effect) or letters (transfer effect). However, the underlying neural mechanisms of this high spatial frequency training improvement remain to be elucidated. In the present study, we examined four properties of neurons in primary visual cortex (area 17) of adult cats that exhibited significantly improved acuity after contrast sensitivity training with a high spatial frequency grating and those of untrained control cats. We found no difference in neuronal contrast sensitivity or tuning width (Width) between the trained and untrained cats. However, the trained cats showed a displacement of the cells’ optimal spatial frequency (OSF) to higher spatial frequencies as well as a larger neuronal signal-to-noise ratio (SNR). Furthermore, both the neuronal differences in OSF and SNR were significantly correlated with the improvement of acuity measured behaviorally. These results suggest that striate neurons might mediate the perceptual learning-induced improvement for high spatial frequency stimuli by an alteration in their spatial frequency representation and by an increased SNR.

Purpose To test the amblyopic suppression at mid to low spatial frequencies when compensating for signal attenuation. Methods Eight amblyopes with (n = 5) or without (n = 3) strabismus and 10 normal controls with normal or corrected to normal visual acuity (≥20/20) and normal stereopsis (≤40 arcseconds) participated. Using a quick contrast sensitivity function approach, we measured individuals' monocular contrast sensitivity functions when the untested eye saw a mean luminance background and when the untested eye saw a bandpass filtered noise whose peak spatial frequency was matched to that of the test grating. Interocular suppression was quantified by the difference in thresholds occurring between these two conditions for each eye. The contrast of the noise mask was set at five times the threshold of the untested eye. Results Selected spatial frequencies (0.67-1.31 cyc/deg) were identified where neither ceiling (five times the mask contrast threshold in the amblyopic eye

To investigate the effect of senescence on signal transmission, we have compared the visual response latency and spontaneous activity of cells in the lateral geniculate nucleus (LGN), area 17, area 18 and posteromedial lateral suprasylvian area (PMLS) of young and old cats. We found that LGN cells in old cats exhibit largely normal visual response latency. In contrast, all the other three areas exhibited significant aging-related delays in the visual response latency. On average, PMLS showed most pronounced delays among these three areas. Area 18 slowed more than area 17, but this was not significant. The degradation of signal timing in the visual cortex might provide insight into neuronal response mechanism underlying perception slowing during aging.

Changes in the visual cortex appear to mediate much of the visual degradation during normal aging. However, how aging affects different stages along the visual pathway is unclear. In the current study, the contrast response function, one of the most important properties of neurons from early visual areas to high brain areas, was systematically compared along the visual pathway, including the lateral geniculate nucleus (LGN), early visual cortices (A17 and A18), and posteromedial lateral suprasylvian cortex (PMLS, analog to the medial temporal area (MT) in monkeys) of young and old cats. We found that the effects of aging on the LGN were negligible, whereas those in the striate cortex were substantial, with even more severe degradation in the PMLS. Reduced contrast sensitivity of neurons in the three cortical areas was accompanied by enhanced maximal visual response, increased spontaneous activity, and decreased signal-to-noise ratio, while LGN neurons exhibited largely normal response properties. Our results suggested that there was a progressively greater effect of aging on neurons at successively higher stages in the visual pathway.

In this research, we compared the visual neuron responses for LGN, A18 and PMLS of old and young cats with extracellular single-neuron recording techniques. We used firing rate vector to characterize information, and response irregularity of cells to evaluate the degeneration of visual characters. Response irregularity is characterized by means of the two coefficients of variation of firing rate vectors: Cv and Cv2. We found that there was no significant change of the response irregularity in LGN areas during the aging process from young to old cats. But in the other two areas, neurons of old cats exhibited significantly larger response irregularity than those of young cats. The result indicated that the information processing function of advanced visual cortex was impaired by aging. This result also provids a reference for the research of the other neuronal system changes during aging process.