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

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 tha...

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Bibliographic Details
Published in:Frontiers in molecular neuroscience 2022-08, Vol.15, p.952782-952782
Main Authors: Sungur, A. Özge, Zeitouny, Caroline, Gabele, Lea, Metz, Isabell, Wöhr, Markus, Michaelsen-Preusse, Kristin, Rust, Marco B.
Format: Article
Language:English
Subjects:
Actin
actin dynamics
Alzheimer's disease
Backbone
Behavior
Dendritic spines
Filaments
Hippocampus
Laboratory animals
memory formation
Morphology
Mutants
Neuropathy
Neuroscience
object recognition
Social behavior
Social interaction
social recognition
Software
spine morphology
ultrasonic vocalization
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Summary: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.
ISSN:1662-5099
1662-5099
DOI:10.3389/fnmol.2022.952782