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Updated: Jul 7, 2026
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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
Published on: October 6, 2017
Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1
Albert Y Hung1, Kensuke Futai, Carlo Sala
1The Institute of Physical and Chemical Research (RIKEN)-Massachusetts Institute of Technology Neuroscience Research Center, Cambridge, Massachusetts 02139, USA.
Summary
Shank1 protein is crucial for synapse structure and function. Shank1 deficiency in mice altered synaptic proteins, spine size, and transmission, impacting anxiety, fear memory, and spatial learning.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Molecular Biology
Background:
- Shank proteins are key postsynaptic scaffold proteins in excitatory synapses.
- Shank3's genetic link to autism suggests Shank proteins' role in cognitive development.
- Experience-dependent changes in dendritic spines are vital for learning and memory.
Purpose of the Study:
- To investigate the in vivo function of Shank1.
- To determine the behavioral and synaptic consequences of Shank1 deficiency.
Main Methods:
- Generation and analysis of Shank1 knock-out mice.
- Assessment of postsynaptic density (PSD) protein composition and dendritic spine morphology.
- Electrophysiological recordings of basal synaptic transmission and plasticity.
- Behavioral testing for anxiety, fear memory, and spatial learning.
Main Results:
- Shank1 mutants exhibited altered PSD composition, reduced dendritic spine size, and diminished basal synaptic transmission.
- Synaptic plasticity remained normal in Shank1-deficient mice.
- Mice lacking Shank1 showed increased anxiety, impaired contextual fear memory, and enhanced spatial learning with deficient long-term retention.
Conclusions:
- Shank1 is essential for maintaining synapse structure and function in vivo.
- Shank1 plays a differential role in specific cognitive processes, potentially relevant to autism spectrum disorders.
