Background: Perceptual profiles, or the performance on visual-perceptual tasks that reflect early visual information processing, have been used to suggest condition-specific visuo-perceptual abilities across neurodevelopmental conditions (NDCs). The complexity-specific hypothesis (Bertone et al., 2010) was based on perceptual profiles defined by a selective decrease in sensitivity to more complex, texture-defined information in adults with autism and fragile-x syndrome, suggesting the atypical development of neural networks underlying early perception in NDCs. The aim of this study was to evaluate whether the complexity-specific hypothesis is applicable to children and adolescents with different NDCs by defining and comparing their perceptual profiles.
Methods: A single interval, two alternative forced-choice identification paradigm was used to measure the perceptual profiles of 64 participants with a NDC (MIQ =78) and 43 typically developing (TD) participants (MIQ =103), aged 5 to 17 years. Participants with a NDC were diagnosed with either: autism spectrum disorder (ASD, n=32), attention deficit/hyperactivity disorder (ADHD, n=9), or intellectual disability (ID, n=12). Perceptual profiles were defined by measuring participants’ sensitivity to static (orientation identification task) and dynamic (direction identification task) gratings (1 cpd) defined by either luminance (simple) or texture (complex) information. The Weschler Abbreviated Scale of Intelligence 2 (WASI-2) was used as a measure of cognitive ability.
Results: When performance was averaged across NDC and TD participants, no between-group difference in sensitivity was found for any of the conditions assessed. However, when assessed as a function of diagnosis, we found that the ID group was less sensitive to both the luminance (P=0.04) and texture-defined (P=0.01) dynamic information when compared to the TD group. Notably, although the perceptual profile of the ASD group was similar of that of the TD group, a significant positive relationship between mental age and sensitivity to both texture-defined static (r=?0.5) and dynamic (r=?0.4) information was found.
Conclusions: The ?ndings demonstrate that different conditions-specific perceptual profiles exist across children and adolescents with different types of NDCs, exemplified by differences found in this study for the ID group. In addition, the positive relationship between perceptual performance and mental age within the ASD group suggests that these perceptual abilities may still be undergoing maturation during the age-range assessed, and provides support for the complexity-specific hypothesis specific to the ASD profile during development. These results exemplify the importance of defining perceptual profiles at different periods of development across NDCs, since the tenets of most perceptually-relevant cognitive theories are based primarily on adult data.
Background: It has been suggested that adaptation to texture density only ever reduces, i.e., never increases, perceived density, implying that density adaptation is ‘uni-directional’ and that texture density is coded as a scalar attribute (Durgin & Huk, 1997). However, we have recently shown that simultaneous density contrast, which describes the effect of a surround texture on the perceived density of a centre region, is ‘bi-directional’—that is, not only do denser surrounds reduce perceived density of the center but sparser surrounds enhance it (Sun, Baker, & Kingdom, 2016). Therefore, we decided to re-examine the directionality of density adaptation.
Methods: We measured the density aftereffect in random dot patterns using a 2AFC matching procedure that established a point-of-subjective-equality (PSE) between an adapted test patch and an unadapted match patch. The adaptors and test were presented at the same position, either at top left or bottom right of the fixation. The match was presented at bottom left or top right correspondingly. These positions were fixed within a block and switched between blocks. Then, using sequential presentation, we measured the density aftereffect for a wide range of adaptor and test densities.
Results: In the first experiment, we observed a unidirectional density aftereffect when test and match were presented simultaneously as in previous studies. However, when they were presented sequentially, bidirectionality was obtained. This bidirectional aftereffect remained when the presentation order of test and match was reversed (second experiment). In the third experiment, we used sequential presentation to measure the density aftereffect for a wide range of adaptor densities (0–73 dots/deg2) and test densities (1.6, 6.4, and 25.6 dots/deg2). We found bidirectionality for all combinations of adaptor and test densities, consistent with our previous SDC results.
Conclusions: In three experiments, we found that density adaptation is bidirectional when the test and match stimuli are presented sequentially. The unidirectional density adaptation reported in previous studies might have been due to effects arising from simultaneous presentation of test and match stimuli. Our evidence again supports the idea that there are density-selective channels in the visual system in line with our previous finding in SDC.
Background: Short-term monocular deprivation has been recently shown to temporarily increase the sensitivity of the patched eye. Many studies have patched subjects for an arbitrary period of 2.5 hours, but for no principled reason. Our goal is to show a relationship, if any, between the length of patching duration and the strength of its effect.
Methods: We tested nine subjects with three different patching durations: 1-, 2-, 3-hour. Four of the nine subjects were patched for 5-hour. Monocular deprivation was achieved by the use of a translucent eyepatch. A session included two rounds of baseline testing of interocular eye balance, patching, and post-patching tests. Each post-patching test occurred at 0, 3, 6, 12, 24, 48, 60 and 96 minutes after patching to track the patching effect over time. Every subject performed two sessions per condition.
Results: One-hour patching produced a small shift in ocular dominance. A larger shift occurred from 2-hour patching, but 3-hour patching produced a comparable effect to the one measured after 2-hour patching.
Conclusions: These results show a saturation of the patching effect beyond 2-hour patching. Hence, we believe that 2-hour patching duration is the optimal duration for eye dominance changes induced by monocular deprivation.
Background: The expression, localization, and function of the endocannabinoid system has been well characterized in recent years in the monkey retina and in the primary thalamic relay, the lateral geniculate nucleus (dLGN). Few data are available on cortical recipients’ structures of the dLGN, namely the primary visual cortex (V1). The goal of this study is to characterize the expression and localization of the metabotropic cannabinoid receptor type 1 (CB1R), the synthesizing enzyme N-acyl phosphatidyl-ethanolamine phospholipase D (NAPE-PLD), and the degradation enzyme fatty acid amide hydrolase (FAAH) in the vervet monkey area V1.
Methods: Using Western blots and immunohistochemistry, we investigated the expression patterns of CB1R, NAPE-PLD, and FAAH in the vervet monkey primary visual cortex.
Results: CB1R, NAPE-PLD, and FAAH were expressed in the primary visual cortex throughout the rostro-caudal axis. CB1R showed very low levels of staining in cortical layer 4, with higher expressions in all other cortical layers, especially layer 1. NAPE-PLD and FAAH expressions were highest in layers 1, 2 and 3, and lowest in layer 4.
Conclusions: Interestingly enough, CB1R was very low in layer 4 of V1 in comparison to the other cortical layers. The visual information coming from the dLGN and entering layer 4Calpha (magno cells) and 4Cbeta (parvo cells) may be therefore modulated by the higher expression levels of CB1R in cortical layers 2 and 3 on the way to the dorsal and ventral visual streams. This is further supported by the higher expression of NAPE-PLD and FAAH in the outer cortical layers. These data indicate that CB1R system can influence the network of activity patterns in the visual stream after the visual information has reached area V1. These novel results provide insights for understanding the role of the endocannabinoids in the modulation of cortical visual inputs, and hence, visual perception.
Background: Visual deficits, caused by ocular disease or trauma to the visual system, can cause lasting damage with insufficient treatment options available. However, recent research has focused on neural plasticity as a means to regain visual abilities. In order to better understand the involvement of neural plasticity and reorganization in partial vision restoration, we aim to evaluate the partial recovery of a visual deficit over time using three behavioural tests. In our study, a partial optic nerve crush (ONC) serves as an induced visual deficit, allowing for residual vision from surviving cells.
Methods: Three behavioural tests—optokinetic reflex, object recognition, and visual cliff—were conducted in 9 mice prior to a bilateral, partial ONC, then 1, 3, 7, 14, 21, and 28 days after the ONC. The optokinetic reflex test measured the tracking reflex in response to moving sinusoidal gratings. These gratings increase in spatial frequency until a reflex is no longer observed, i.e., a visual acuity threshold is reached. The object recognition test examines the animal’s exploratory behaviour in its capacity to distinguish high versus low contrast objects. The visual cliff test also evaluates exploratory behaviour, by simulating a cliff to observe the animal’s sense of depth perception. All three tests provide an estimate of the rodent’s visual abilities at different levels of the visual pathway.
Results: The partial optic nerve crush resulted in a total loss of visual acuity as measured by the optokinetic reflex. The deficit did not show improvement during the 4 following weeks. Despite the visual cliff test showing a non-significant decrease in deep end preference 1-day post ONC, though this was not the case for subsequent test occasions. The object recognition test showed no significant trends.
Conclusions: In conclusion, the optokinetic reflex test showed a significant loss of function following the visual deficit, but no recovery. However, a complimentary pilot study shows visual recovery using lighter crush intensities. The spatial visual function does not seem to be affected by the ONC, suggesting that the object recognition and visual cliff tests, in their current design, may rely on somatosensory means of exploration.
Background: Research suggests that the analysis of facial expressions by a healthy brain would take place approximately 170 ms after the presentation of a facial expression in the superior temporal sulcus and the fusiform gyrus, mostly in the right hemisphere. Some researchers argue that a fast pathway through the amygdala would allow automatic and early emotional treatment around 90 ms after stimulation. This treatment would be done subconsciously, even before this stimulus is perceived and could be approximated by presenting the stimuli quickly on the periphery of the fovea. The present study aimed to identify the neural correlates of a peripheral and simultaneous presentation of emotional expressions through a frequency tagging paradigm.
Methods: The presentation of emotional facial expressions at a specific frequency induces in the visual cortex a stable and precise response to the presentation frequency [i.e., a steady-state visual evoked potential (ssVEP)] that can be used as a frequency tag (i.e., a frequency-tag to follow the cortical treatment of this stimulus. Here, the use of different specific stimulation frequencies allowed us to label the different facial expressions presented simultaneously and to obtain a reliable cortical response being associated with (I) each of the emotions and (II) the different times of presentations repeated (1/0.170 ms =~5.8 Hz, 1/0.090 ms =~10.8 Hz). To identify the regions involved in emotional discrimination, we subtracted the brain activity induced by the rapid presentation of six emotional expressions of the activity induced by the presentation of the same emotion (reduced by neural adaptation). The results were compared to the hemisphere in which attention was sought, emotion and frequency of stimulation.
Results: The signal-to-noise ratio of the cerebral oscillations referring to the treatment of the expression of fear was stronger in the regions specific to the emotional treatment when they were presented in the subjects peripheral vision, unbeknownst to them. In addition, the peripheral emotional treatment of fear at 10.8 Hz was associated with greater activation within the Gamma 1 and 2 frequency bands in the expected regions (frontotemporal and T6), as well as desynchronization in the Alpha frequency bands for the temporal regions. This modulation of the spectral power is independent of the attentional request.
Conclusions: These results suggest that the emotional stimulation of fear presented in the peripheral vision and outside the attentional framework elicit an increase in brain activity, especially in the temporal lobe. The localization of this activity as well as the optimal stimulation frequency found for this facial expression suggests that it is treated by the fast pathway of the magnocellular layers.
Background: Exposure to ethanol in utero leads to several brain development disorders including retinal abnormalities whose underlying cellular pathogenesis remains elusive. We have previously reported changes in electroretinogram recordings in moderate fetal alcohol exposure (MFAE) vervet monkeys. The goal of this study is to characterize the anatomical effects of moderate MFAE during the third trimester in the vervet monkey retina.
Methods: Using immunohistochemistry and Western blots, we analyzed changes in the expression of cell-type specific proteins that may occur in the MFAE retina compared to the normal retina. We also compared the basic retinal anatomy across groups by examining retinal layering and thickness.
Results: Our main result indicates that GFAP (a potent marker of astrocytes) immunoreactivity was increased in the MFAE retina indicating strong astrogliosis. There was no obvious change in the overall anatomy in the MFAE retina and no significant differences in the mean thickness of each retinal layer. Furthermore, no significant changes in the morphology of the photoreceptors, horizontal cells, bipolar cells, and amacrines cells was observed.
Conclusions: These data indicate that astrogliosis is a consequence of prenatal alcohol exposure and might explain the reported changes in the electroretinographic responses.
Background: Rods and cones are critical for light detection. Although there has been considerable work done in elucidating the molecular mechanisms involved in rod development, not much is known about how the cone cell fate decision is made by the multipotent retinal progenitor cells during development. Analysis of the promoter regions of Nrl and trβ2, rod and cone differentiation factors respectively, revealed DNA binding motifs of two POU-domain containing transcription factors, Pou2f1 and Pou2f2. Preliminary experiments showed that Pou2f1/2 are expressed during the peak of cone genesis in the embryonic retina. Therefore, we hypothesize that Pou2f1/2 specify cone cell fate in the developing retina.
Methods: We used immunofluorescence and in situ hybridization to establish the spatiotemporal expression of Pou2f1/2 during retinogenesis. We performed in vivo electroporation in post-natal mice to misexpress Pou2f1/2 and used antibodies specific to proteins expressed in cones such as Rxrγ and S-opsin to count cones. Using ex vivo electroporation of embryonic retinal explants, we knocked out Pou2f1 and Pou2f2 using CRISPR/Cas9 gRNAs at the peak of cone production window. Finally, we transfected post-natal retinal explants with a combination of regulatory elements of Nrl or thrb with control backbone vector, Pou2f1 or Pou2f2 using electroporation.
Results: We found that Pou2f1/2 are expressed in retinal progenitor cells in the developing retina and subsequently in the differentiated cones. Pou2f1/2 misexpression outside the cone genesis window led to an increase in cones at the expense of rods. Pou2f1/2 indel knockouts generated by CRISPR/Cas9 gRNAs led to a decrease in cones and a converse increase in rods. Finally, we found that Pou2f1/2 activate the cis-regulatory module (CRM) of the thrb gene and repress the activity of the CRM of Nrl.
Conclusions: These results uncover novel players that establish the complex gene regulatory network for cone photoreceptor fate specification in the retinal progenitor cells. We anticipate that this work should help us devise improved replacement therapies in the future utilizing stem cells for retinal degenerative diseases such as aged-related macular degeneration (AMD) and Stargardt’s disease.
Background: Decrease of ocular blood flow has been linked to the pathogenesis of ocular diseases such as glaucoma and age-related macular degeneration. Current methods that measure the pulsatile blood flow have major limitations, including the assumption that ocular rigidity is the same in all eyes. Our group has recently developed a new method to measure the pulsatile choroidal volume change by direct visualization of the choroid with OCT imaging and automated segmentation. Our goal in this study is to describe the distribution of PCBF in a healthy Caucasian population.
Methods: Fifty-one subjects were recruited from the Maisonneuve-Rosemont Hospital Ophthalmology Clinic and underwent PCBF measurement in one eye. The distribution of PCBF in healthy eyes was assessed.
Results: The distribution of PCBF among the healthy eyes was found to be 3.94±1.70 μL with this technique.
Conclusions: This study demonstrates the normal range of PCBF values obtained in a healthy Caucasian population. This technique could be used for further investigation of choroid pulsatility and to study glaucoma pathophysiology.
