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Autistic-like behaviours and hyperactivity in mice lacking ProSAP1/Shank2.

Michael J Schmeisser1, Elodie Ey, Stephanie Wegener

  • 1Institute for Anatomy and Cell Biology, Ulm University, 89081 Ulm, Germany.

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|June 16, 2012
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Genetic deletion of ProSAP1/Shank2 in mice caused autism-like behaviors and synaptic changes. Different Shank protein deficits may underlie distinct autism spectrum disorder phenotypes, suggesting tailored therapies.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Autism spectrum disorders (ASDs) involve social deficits and repetitive behaviors.
  • Mutations in synaptic proteins are linked to ASDs, but mechanisms are unclear.
  • ProSAP/Shank proteins organize postsynaptic density at excitatory synapses.

Purpose of the Study:

  • Investigate the role of ProSAP1/Shank2 in synaptic function and behavior.
  • Determine the impact of ProSAP1/Shank2 deletion on glutamate receptor expression.
  • Compare ProSAP1/Shank2 deficits with ProSAP2/Shank3 to understand ASD heterogeneity.

Main Methods:

  • Generated ProSAP1/Shank2 knockout mice (ProSAP1/Shank2(-/-)).
  • Analyzed synaptic changes, including ionotropic glutamate receptor expression and dendritic spines.
  • Assessed synaptic transmission and N-methyl-d-aspartate receptor currents.
  • Evaluated behavioral alterations such as hyperactivity and social deficits.

Main Results:

  • ProSAP1/Shank2 deletion led to brain-region-specific upregulation of ionotropic glutamate receptors.
  • Mutant mice showed reduced dendritic spines, impaired synaptic transmission, and altered excitatory currents.
  • ProSAP1/Shank2(-/-) mutants exhibited hyperactivity, repetitive grooming, and social/vocal abnormalities.
  • Distinct Shank protein deficits resulted in different synaptic and behavioral phenotypes.

Conclusions:

  • ProSAP1/Shank2 plays a crucial role in synaptic organization and function.
  • Altered synaptic glutamate receptor expression is a key mechanism in ASD.
  • Tailoring therapies to specific synaptopathic phenotypes is essential for effective ASD treatment.