Transient reduction in dendritic spine density in brain-specific profilin1 mutant mice is associated with behavioral deficits

A Özge Sungur; Caroline Zeitouny; Lea Gabele; Isabell Metz; Markus Wöhr; Kristin Michaelsen-Preusse; Marco B Rust

doi:10.3389/fnmol.2022.952782

Transient reduction in dendritic spine density in brain-specific profilin1 mutant mice is associated with behavioral deficits

Front Mol Neurosci. 2022 Aug 3:15:952782. doi: 10.3389/fnmol.2022.952782. eCollection 2022.

Authors

A Özge Sungur^{1

2}, Caroline Zeitouny³, Lea Gabele³, Isabell Metz^{1

4}, Markus Wöhr^{2

5

6}, Kristin Michaelsen-Preusse³, Marco B Rust^{1

4

7}

Affiliations

¹ Molecular Neurobiology Group, Institute of Physiological Chemistry, University of Marburg, Marburg, Germany.
² Behavioral Neuroscience, Experimental and Biological Psychology, University of Marburg, Marburg, Germany.
³ Department of Cellular Neurobiology, Technical University (TU) Braunschweig, Braunschweig, Germany.
⁴ Deutsche Forschungsgemeinschaft (German Research Foundation) (DFG) Research Training Group, Membrane Plasticity in Tissue Development and Remodeling, Graduiertenkolleg (Gradeschool) (GRK) 2213, University of Marburg, Marburg, Germany.
⁵ Social and Affective Neuroscience Research Group, Laboratory of Biological Psychology, Research Unit Brain and Cognition, Faculty of Psychology and Educational Sciences, Katholeike Universiteit (KU) Leuven, Leuven, Belgium.
⁶ Leuven Brain Institute, Katholeike Universiteit (KU) Leuven, Leuven, Belgium.
⁷ Center for Mind, Brain and Behavior (CMBB), University of Marburg and Justus-Liebig-University Giessen, Marburg, Germany.

Abstract

Actin filaments form the backbone of dendritic spines, the postsynaptic compartment of most excitatory synapses in the brain. Spine density changes affect brain function, and postsynaptic actin defects have been implicated in various neuropathies. It is mandatory to identify the actin regulators that control spine density. Based on previous studies, we hypothesized a role for the actin regulator profilin1 in spine formation. We report reduced hippocampal spine density in juvenile profilin1 mutant mice together with impairments in memory formation and reduced ultrasonic communication during active social behavior. Our results, therefore, underline a previously suggested function of profilin1 in controlling spine formation and behavior in juvenile mice.

Keywords: actin dynamics; memory formation; object recognition; social recognition; spine morphology; ultrasonic vocalization.