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Conditional deletion of ROCK2 induces anxiety-like behaviors and alters dendritic spine density and morphology on CA1 pyramidal neurons

Summary

Researchers created mice with reduced ROCK2 protein in brain cells to understand how this protein affects behavior and brain structure. These mice showed anxiety-like behavior, avoiding open spaces and preferring darkness. The study found that ROCK2 affects the structure of dendritic spines, which are tiny branches on nerve cells that allow communication between neurons, particularly in the hippocampus region involved in learning and memory.

Background

ROCK2 is an attractive drug target for neurologic disorders, but lacks a mouse model enabling spatial and temporal control of gene expression. ROCK1 and ROCK2 are serine/threonine kinases that regulate actin-myosin cytoskeleton contractility and are involved in cellular morphology and motility.

Objective

To investigate the contribution of ROCK2 in behavior and dendritic spine morphology in the hippocampus, medial prefrontal cortex, and basolateral amygdala using conditional ROCK2 knockout mice with CaMKII-Cre expression in forebrain excitatory neurons.

Results

Cre/ROCK2 fl/fl mice exhibited anxiety-like behaviors with reduced time in open arms of elevated plus maze and increased time in dark environments. In dorsal CA1, increased thin spine density on basal dendrites and reduced spine head volume on apical dendrites were observed. In ventral CA1, increased spine length on apical dendrites was noted. Spine morphology in mPFC and BLA was unchanged.

Conclusion

ROCK2 deficiency in forebrain excitatory neurons mediates spine density and morphology in a compartmentalized manner within CA1 pyramidal cells, suggesting these structural changes may contribute to anxiety-like behaviors. The findings indicate regional and compartment-specific roles for ROCK2 in hippocampal structural plasticity.
  • Published in:Molecular Brain,
  • Study Type:Animal Research Study,
  • Source: PMC8600782, PMID: 34794469, DOI: 10.1186/s13041-021-00878-4
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