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Abstract
Muskelin (Mkln1) is implicated in neuronal function, regulating plasma membrane receptor trafficking. However, its influence on intrinsic brain activity and corresponding behavioral processes remains unclear. Here we show that murine Mkln1 knockout causes non-habituating locomotor activity, increased exploratory drive, and decreased locomotor response to amphetamine. Muskelin deficiency impairs social novelty detection while promoting the retention of spatial reference memory and fear extinction recall. This is strongly mirrored in either weaker or stronger resting-state functional connectivity between critical circuits mediating locomotor exploration and cognition. We show that Mkln1 deletion alters dendrite branching and spine structure, coinciding with enhanced AMPAR-mediated synaptic transmission but selective impairment in synaptic potentiation maintenance. We identify muskelin at excitatory synapses and highlight its role in regulating dendritic spine actin stability. Our findings point to aberrant spine actin modulation and changes in glutamatergic synaptic function as critical mechanisms that contribute to the neurobehavioral phenotype arising from Mkln1 ablation.
A murine muskelin knockout induces increased exploratory drive and alters cognition and functional connectivity. These effects correlate with actin-dependent changes in dendritic branching, spine structure, and AMPAR-mediated synaptic transmission.
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1 Institute of Molecular Neurogenetics, Center for Molecular Neurobiology, ZMNH, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (GRID:grid.13648.38) (ISNI:0000 0001 2180 3484); Institute of Science and Technology (IST) Austria, Klosterneuburg, Austria (GRID:grid.33565.36) (ISNI:0000000404312247)
2 RG Neuroplasticity Leibniz Institute for Neurobiology, Magdeburg, Germany (GRID:grid.418723.b) (ISNI:0000 0001 2109 6265)
3 University Medical Center Hamburg-Eppendorf, Department of Diagnostic and Interventional Neuroradiology, Hamburg, Germany (GRID:grid.13648.38) (ISNI:0000 0001 2180 3484); Centre for the Developing Brain, School of Biomedical Engineering & Imaging Sciences, King’s College London, Biomedical Engineering Department, London, UK (GRID:grid.13097.3c) (ISNI:0000 0001 2322 6764)
4 Institute of Molecular Neurogenetics, Center for Molecular Neurobiology, ZMNH, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (GRID:grid.13648.38) (ISNI:0000 0001 2180 3484)
5 RG Neuroplasticity Leibniz Institute for Neurobiology, Magdeburg, Germany (GRID:grid.418723.b) (ISNI:0000 0001 2109 6265); Leibniz Group ‘Dendritic Organelles and Synaptic Function’, Center for Molecular Neurobiology, ZMNH, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (GRID:grid.13648.38) (ISNI:0000 0001 2180 3484)