Faculty Opinions recommendation of Ube3a loss increases excitability and blunts orientation tuning in the visual cortex of Angelman syndrome model mice.

2017 ◽  
Author(s):  
Hans van Bokhoven
Keyword(s):  
Visual Cortex ◽  
Angelman Syndrome ◽  
Orientation Tuning

scholarly journals Ube3a loss increases excitability and blunts orientation tuning in the visual cortex of Angelman syndrome model mice

2017 ◽  
Vol 118 (1) ◽  
pp. 634-646 ◽  
Author(s):  
Michael L. Wallace ◽  
Geeske M. van Woerden ◽  
Ype Elgersma ◽  
Spencer L. Smith ◽  
Benjamin D. Philpot
Keyword(s):  
Visual Cortex ◽  
Angelman Syndrome ◽  
Pyramidal Neurons ◽  
Neurodevelopmental Disorder ◽  
Inhibitory Neurons ◽  
Electrophysiological Recording ◽  
Orientation Tuning ◽  
Visual Cortical ◽  
Deficient Mice

Angelman syndrome (AS) is a neurodevelopmental disorder caused by loss of the maternally inherited allele of UBE3A. Ube3aSTOP/p+ mice recapitulate major features of AS in humans and allow conditional reinstatement of maternal Ube3a with the expression of Cre recombinase. We have recently shown that AS model mice exhibit reduced inhibitory drive onto layer (L)2/3 pyramidal neurons of visual cortex, which contributes to a synaptic excitatory/inhibitory imbalance. However, it remains unclear how this loss of inhibitory drive affects neural circuits in vivo. Here we examined visual cortical response properties in individual neurons to explore the consequences of Ube3a loss on intact cortical circuits and processing. Using in vivo patch-clamp electrophysiology, we measured the visually evoked responses to square-wave drifting gratings in L2/3 regular-spiking (RS) neurons in control mice, Ube3a-deficient mice, and mice in which Ube3a was conditionally reinstated in GABAergic neurons. We found that Ube3a-deficient mice exhibited enhanced pyramidal neuron excitability in vivo as well as weaker orientation tuning. These observations are the first to show alterations in cortical computation in an AS model, and they suggest a basis for cortical dysfunction in AS. NEW & NOTEWORTHY Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by the loss of the gene UBE3A. Using electrophysiological recording in vivo, we describe visual cortical dysfunctions in a mouse model of AS. Aberrant cellular properties in AS model mice could be improved by reinstating Ube3a in inhibitory neurons. These findings suggest that inhibitory neurons play a substantial role in the pathogenesis of AS.

Effects of Feedback Projections From Area 18 Layers 2/3 to Area 17 Layers 2/3 in the Cat Visual Cortex

1999 ◽  
Vol 82 (5) ◽  
pp. 2667-2675 ◽  
Author(s):  
Susana Martinez-Conde ◽  
Javier Cudeiro ◽  
Kenneth L. Grieve ◽  
Rosa Rodriguez ◽  
Casto Rivadulla ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Small Region ◽  
Orientation Tuning ◽  
Area 17 ◽  
Visual Responses ◽  
Area 18 ◽  
Cat Visual Cortex ◽  
Effects Of Feedback ◽  
Feedback Connections

In the absence of a direct geniculate input, area 17 cells in the cat are nevertheless able to respond to visual stimuli because of feedback connections from area 18. Anatomic studies have shown that, in the cat visual cortex, layer 5 of area 18 projects to layer 5 of area 17, and layers 2/3 of area 18 project to layers 2/3 of area 17. What is the specific role of these connections? Previous studies have examined the effect of area 18 layer 5 blockade on cells in area 17 layer 5. Here we examine whether the feedback connections from layers 2/3 of area 18 influence the orientation tuning and velocity tuning of cells in layers 2/3 of area 17. Experiments were carried out in anesthetized and paralyzed cats. We blocked reversibly a small region (300 μm radius) in layers 2/3 of area 18 by iontophoretic application of GABA and recorded simultaneously from cells in layers 2/3 of area 17 while stimulating with oriented sweeping bars. Area 17 cells showed either enhanced or suppressed visual responses to sweeping bars of various orientations and velocities during area 18 blockade. For most area 17 cells, orientation bandwidths remained unaltered, and we never observed visual responses during blockade that were absent completely in the preblockade condition. This suggests that area 18 layers 2/3 modulate visual responses in area 17 layers 2/3 without fundamentally altering their specificity.

scholarly journals Traumatic brain injury to primary visual cortex produces long-lasting circuit dysfunction

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Jan C. Frankowski ◽  
Andrzej T. Foik ◽  
Alexa Tierno ◽  
Jiana R. Machhor ◽  
David C. Lyon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Visual Cortex ◽  
Brain Injury ◽  
Primary Visual Cortex ◽  
Visual Stimuli ◽  
Orientation Tuning ◽  
V1 Neurons ◽  
Adult Mice ◽  
Electrophysiological Recordings

AbstractPrimary sensory areas of the mammalian neocortex have a remarkable degree of plasticity, allowing neural circuits to adapt to dynamic environments. However, little is known about the effects of traumatic brain injury on visual circuit function. Here we used anatomy and in vivo electrophysiological recordings in adult mice to quantify neuron responses to visual stimuli two weeks and three months after mild controlled cortical impact injury to primary visual cortex (V1). We found that, although V1 remained largely intact in brain-injured mice, there was ~35% reduction in the number of neurons that affected inhibitory cells more broadly than excitatory neurons. V1 neurons showed dramatically reduced activity, impaired responses to visual stimuli and weaker size selectivity and orientation tuning in vivo. Our results show a single, mild contusion injury produces profound and long-lasting impairments in the way V1 neurons encode visual input. These findings provide initial insight into cortical circuit dysfunction following central visual system neurotrauma.

scholarly journals The Development of Active Binocular Vision under Normal and Alternate Rearing Conditions

2020 ◽  
Author(s):  
Lukas Klimmasch ◽  
Johann Schneider ◽  
Alexander Lelais ◽  
Bertram E. Shi ◽  
Jochen Triesch
Keyword(s):  
Visual Cortex ◽  
Binocular Vision ◽  
Cortical Neurons ◽  
Orientation Tuning ◽  
Active Perception ◽  
Efficient Coding ◽  
Rearing Conditions ◽  
Active Binocular Vision ◽  
Experimental Findings ◽  
Visual Cortical

AbstractThe development of binocular vision is an active learning process comprising the development of disparity tuned neurons in visual cortex and the establishment of precise vergence control of the eyes. We present a computational model for the learning and self-calibration of active binocular vision based on the Active Efficient Coding framework, an extension of classic efficient coding ideas to active perception. Under normal rearing conditions, the model develops disparity tuned neurons and precise vergence control, allowing it to correctly interpret random dot stereogramms. Under altered rearing conditions modeled after neurophysiological experiments, the model qualitatively reproduces key experimental findings on changes in binocularity and disparity tuning. Furthermore, the model makes testable predictions regarding how altered rearing conditions impede the learning of precise vergence control. Finally, the model predicts a surprising new effect that impaired vergence control affects the statistics of orientation tuning in visual cortical neurons.

scholarly journals Temporo-nasally biased moving grating selectivity in mouse primary visual cortex

2019 ◽  
Author(s):  
Marie Tolkiehn ◽  
Simon R. Schultz
Keyword(s):  
Visual Cortex ◽  
Spatial Frequency ◽  
Primary Visual Cortex ◽  
Moving Objects ◽  
Direction Selectivity ◽  
Orientation Tuning ◽  
High Signal ◽  
Forward Movement ◽  
Upward Moving

AbstractOrientation tuning in mouse primary visual cortex (V1) has long been reported to have a random or “salt-and-pepper” organisation, lacking the structure found in cats and primates. Laminar in-vivo multi-electrode array recordings here reveal previously elusive structure in the representation of visual patterns in the mouse visual cortex, with temporo-nasally drifting gratings eliciting consistently highest neuronal responses across cortical layers and columns, whilst upward moving gratings reliably evoked the lowest activities. We suggest this bias in direction selectivity to be behaviourally relevant as objects moving into the visual field from the side or behind may pose a predatory threat to the mouse whereas upward moving objects do not. We found furthermore that direction preference and selectivity was affected by stimulus spatial frequency, and that spatial and directional tuning curves showed high signal correlations decreasing with distance between recording sites. In addition, we show that despite this bias in direction selectivity, it is possible to decode stimulus identity and that spatiotemporal features achieve higher accuracy in the decoding task whereas spike count or population counts are sufficient to decode spatial frequencies implying different encoding strategies.Significance statementWe show that temporo-nasally drifting gratings (i.e. opposite the normal visual flow during forward movement) reliably elicit the highest neural activity in mouse primary visual cortex, whereas upward moving gratings reliably evoke the lowest responses. This encoding may be highly behaviourally relevant, as objects approaching from the periphery may pose a threat (e.g. predators), whereas upward moving objects do not. This is a result at odds with the belief that mouse primary visual cortex is randomly organised. Further to this biased representation, we show that direction tuning depends on the underlying spatial frequency and that tuning preference is spatially correlated both across layers and columns and decreases with cortical distance, providing evidence for structural organisation in mouse primary visual cortex.

Bicuculline and orientation tuning of neurons of the visual cortex

1996 ◽  
Vol 27 (1) ◽  
pp. 42-49 ◽  
Author(s):  
N. A. Lazareva ◽  
I. A. Shevelev ◽  
U. T. Eysel ◽  
G. A. Sharaev
Keyword(s):  
Visual Cortex ◽  
Orientation Tuning
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