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Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent Visual Cortex
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.
HCN channelopathy and auditory hypersensitivity in the Shank3 mouse model of ASD
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
Combined expansion and STED microscopy reveals fingerprints of synaptic nanostructure across brain regions and in ASD-related SHANK3 deficiency
FENS Forum 2024
Dysregulation of vasopressin release from the bed nucleus of stria terminalis to the lateral septum promotes social deficits in Shank3B+/- mice
FENS Forum 2024
Early cortical network deficits underlying abnormal stimulus perception in Shank3b+/- mice
FENS Forum 2024
From systems biology to drug targets: ATP synthase subunit upregulation causes mitochondrial dysfunction in Shank3Δ4-22 mouse model of autism
FENS Forum 2024
The impact of Shank3 postsynaptic protein deficiency on neuronal synaptic activity in the striatum of an autism-related mouse model
FENS Forum 2024
Modulation of sensory deficits in Shank3b mice through cathodal tDCS
FENS Forum 2024
Quantifying social behaviors in juvenile Shank3 mice using animal pose estimation tools
FENS Forum 2024
SHANK3 deficiency leads to GABAergic abnormalities and morphological changes in somatostatin-expressing interneurons in olfactory brain regions
FENS Forum 2024
Tactile sensory processing deficits in the Shank3 KO mouse model of autism spectrum disorder
FENS Forum 2024
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