TopicNeuroscience

shank3

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SeminarNeuroscience

Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent Visual Cortex

Gina Turrigiano

Brandeis University

Jul 21, 2020

Neocortical networks must generate and maintain stable activity patterns despite perturbations induced by learning and experience- dependent plasticity. There is abundant theoretical and experimental evidence that network stability is achieved through homeostatic plasticity mechanisms that adjust synaptic and neuronal properties to stabilize some measure of average activity, and this process has been extensively studied in primary visual cortex (V1), where chronic visual deprivation induces an initial drop in activity and ensemble average firing rates (FRs), but over time activity is restored to baseline despite continued deprivation. Here I discuss recent work from the lab in which we followed this FR homeostasis in individual V1 neurons in freely behaving animals during a prolonged visual deprivation/eye-reopening paradigm. We find that - when FRs are perturbed by manipulating sensory experience - over time they return precisely to a cell-autonomous set-point. Finally, we find that homeostatic plasticity is perturbed in a mouse model of Autism spectrum disorder, and this results in a breakdown of FRH within V1. These data suggest that loss of homeostatic plasticity is one primary cause of excitation/inhibition imbalances in ASD models. Together these studies illuminate the role of stabilizing plasticity mechanisms in the ability of neocortical circuits to recover robust function following challenges to their excitability.

shank3

Latest

Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent Visual Cortex

DIFFERENTIAL GENOTYPE-PHENOTYPE CORRELATION ACROSS SOCIAL AND SENSORY DOMAINS IN THE HETEROZYGOUS SHANK3B MOUSE MODEL OF AUTISM SPECTRUM DISORDER

EARLY DEVELOPMENTAL STRUCTURAL AND FUNCTIONAL ALTERATIONS IN HIPPOCAMPAL CA1 IN <EM>SHANK3</EM> MUTANT MICE

EARLY ONSET OF CEREBELLAR AND PERIPHERAL INFLAMMATION IN CNTNAP2 AND SHANK3B MOUSE MODELS OF AUTISM

ALTERED CORTEX-WIDE SPONTANEOUS DYNAMICS ACCOMPANY ENHANCED SENSORY RESPONSE AMPLITUDE AND VARIABILITY IN SHANK3B MICE

THALAMOCORTICAL ENCODING OF TACTILE STIMULI IN THE <EM>SHANK3 </EM>KO MOUSE MODEL OF AUTISM SPECTRUM DISORDER

DISRUPTED THALAMIC ENCODING OF TACTILE PROCESSING IN JUVENILE SHANK3B MUTANT MICE

GENE X ENVIRONMENT INTERACTION IN A NEURONAL MODEL OF SHANK3-RELATED AUTISM SPECTRUM DISORDER

ALTERED CORTEX-WIDE DYNAMICS DISRUPT MOTOR PLANNING IN SHANK3-MUTANT MICE

Combined expansion and STED microscopy reveals fingerprints of synaptic nanostructure across brain regions and in ASD-related SHANK3 deficiency

Dysregulation of vasopressin release from the bed nucleus of stria terminalis to the lateral septum promotes social deficits in Shank3B+/- mice

Early cortical network deficits underlying abnormal stimulus perception in Shank3b+/- mice

From systems biology to drug targets: ATP synthase subunit upregulation causes mitochondrial dysfunction in Shank3Δ4-22 mouse model of autism

The impact of Shank3 postsynaptic protein deficiency on neuronal synaptic activity in the striatum of an autism-related mouse model

Modulation of sensory deficits in Shank3b mice through cathodal tDCS

Quantifying social behaviors in juvenile Shank3 mice using animal pose estimation tools

SHANK3 deficiency leads to GABAergic abnormalities and morphological changes in somatostatin-expressing interneurons in olfactory brain regions

HCN channelopathy and auditory hypersensitivity in the Shank3 mouse model of ASD

Tactile sensory processing deficits in the Shank3 KO mouse model of autism spectrum disorder

KIAA1217 as a novel synaptic protein that interacts with PSD95 and Shank3 and controls dendritic spine plasticity

Mice models and autism spectrum disorders : the example of the Shank3Δ11/Δ 11 mouse

Quantifying social behaviors in juvenile Shank3 mice using animal pose estimation tools

Somatosensory processing deficits and altered cortico-hippocampal connectivity in Shank3b−/− mice

Striatal dysfunctions with aging in Shank3 KO mouse model of autism spectrum disorders

Mice models and autism spectrum disorders : the example of the Shank3Δ11/Δ 11 mouse