Differences in orientation tuning between pinwheel and domain neurons in primary visual cortex depend on contrast and size

Liu, Yong-Jun; Hashemi-Nezhad, Maziar; Lyon, David C.

doi:10.1117/1.nph.4.3.031209

Cited by 5 publications

(2 citation statements)

References 72 publications

(123 reference statements)

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“…For orientation, the tuning width (HWHH) of the preferred orientation is more than twice as sharp in the control example (24.3º vs 48.9º;Fig 4A,B), and this difference is also seen for the population (Control: 27.7º ± 2.4, compared to 47.9º ± 4.4 in CCI injured animals; P = 0.0009;Fig 4C). Broader tuning after TBI is consistent with orientation tuning mediated more through feedforward mechanisms and impairments in cortical inhibition(Liu et al, 2015;Liu et al, 2017). Similarly, the larger size preference in TBI compared to control neuron examples (73º vs. 35º;Fig 4D,E)and populations (52 ± 5 º, compared to 32 ± 3 º; P = 0.005;Fig 4F)also indicates a loss of cortical inhibition(Liu et al, 2011).…”

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Primary visual cortex injury produces loss of inhibitory neurons and long-term visual circuit dysfunction

Frankowski¹,

Foik

Machhor³

et al. 2020

Preprint

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Primary 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 effect of traumatic brain injury on visual system function. Here we applied a mild focal contusion injury to primary visual cortex (V1) in adult mice. We found that, although V1 was largely intact in brain-injured mice, there was a reduction in the number of inhibitory interneurons that extended into deep cortical layers. In general, we found a preferential reduction of interneurons located in superficial layers, near the impact site, while interneurons positioned in deeper layers were better preserved. Three months after injury, V1 neurons showed dramatically reduced responses to visual stimuli and weaker orientation selectivity and tuning, consistent with the loss of cortical inhibition. Our results demonstrate that V1 neurons no longer robustly and stably encode visual input following a mild traumatic injury.

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confidence: 58%

“…al., 2011; Liu et al,2015;Liu et al, 2017). For orientation, the tuning width (HWHH) of the preferred orientation is more than twice as sharp in the control example (24.3º vs 48.9º;Fig 4A,B), and this difference is also seen for the population (Control: 27.7º ± 2.4, compared to 47.9º ± 4.4 in CCI injured animals; P = 0.0009;Fig 4C).…”

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confidence: 99%

Primary visual cortex injury produces loss of inhibitory neurons and long-term visual circuit dysfunction

Frankowski¹,

Foik

Machhor³

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

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

et al. 2021

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Primary 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.

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Adaptation-induced plasticity in the sensory cortex

Bharmauria

Ouelhazi

Lussiez

et al. 2022

Journal of Neurophysiology

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For medical and fundamental reasons, we need to understand adult brain plasticity at several levels: structural, physiological, and behavioural. Historically, brain plasticity has been mostly investigated by weakening or removing sensory inputs. The visual system has been extensively used because diminishing visual inputs - i.e., visual deprivation-induced plasticity - permits more tractable findings. The present review is centered on the reverse strategy, by imposing a novel stimulus - i.e., adaptation-induced plasticity. Adaptation refers to the constant (milliseconds to hours) presentation of a non-optimal stimulus (adapter) within the receptive field (RF, spatial area that modulates neuronal firing) of the neuron under observation. We specifically focus on how adaptation impacts the tuning of visual neurons with other associated properties. After adaptation, visual cortical neurons respond robustly to the adapter (pre-adaptation it typically evokes feeble responses) by developing alternate tuning curves that outlast the adaptation time. Here, with dendritic structure as foundation, we synthesize a push-pull mechanism of development and acquisition of novel tuning curves following adaptation. We then explain how these changes apply at the global level across different brain regions and species with a short description of underlying neurochemical changes. Finally, we discuss physiopathological consequences and conclude with some gaps and questions that need to be addressed to further comprehend such neuroplasticity.

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Differences in orientation tuning between pinwheel and domain neurons in primary visual cortex depend on contrast and size

Cited by 5 publications

References 72 publications

Primary visual cortex injury produces loss of inhibitory neurons and long-term visual circuit dysfunction

Primary visual cortex injury produces loss of inhibitory neurons and long-term visual circuit dysfunction

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

Adaptation-induced plasticity in the sensory cortex

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