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Behavioral abnormalities in mice lacking mesenchyme-specific Pten.

Jeremy C Borniger¹, Yasmine M Cissé¹, Carmen Z Cantemir-Stone¹

¹Department of Neuroscience and the Behavioral Neuroendocrinology Group, The Ohio State University-Wexner Medical Center, Columbus, OH 43210, USA.

Behavioural Brain Research

|February 16, 2016

Summary

This summary is machine-generated.

Loss of Phosphatase and tensin homolog (Pten) in brain astrocytes did not significantly alter social or anxiety-like behaviors in mice. These findings suggest neuronal Pten is critical for these behavioral phenotypes.

Keywords:

Astrocytes Behavior FSP1 Hippocampus Pten S100A4

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Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Phosphatase and tensin homolog (Pten) acts as a negative regulator of cell proliferation and growth.
Central nervous system (CNS)-specific Pten deletion impacts social and anxiety-related behaviors.
Fibroblast-specific protein 1 (Fsp1), also known as S100A4, is a mesenchymal marker expressed in astrocytes.

Purpose of the Study:

To investigate the behavioral effects of Pten deletion in Fsp1-expressing cells within the CNS.
To determine if Pten loss in astrocytes influences social interaction and anxiety-like behaviors.
To assess the potential of environmental enrichment to mitigate genetic behavioral deficits.

Main Methods:

Utilized a Cre-recombinase approach with Lox sequences to delete Pten (exons 4-5) in Fsp1-positive cells.
Employed a β-galactosidase Rosa26(LoxP) reporter allele to track expression sites.
Conducted a comprehensive battery of behavioral assays on Fsp1-Cre;Pten(LoxP/LoxP) mice (Pten(-/-)) and Pten(LoxP/LoxP) controls (Pten(+/+)).

Main Results:

Pten deletion occurred throughout the brain parenchyma and pituitary in Fsp1-positive cells.
Despite physical differences like reduced hippocampal size and sensorimotor deficits, Pten(-/-) mice showed minimal behavioral alterations compared to controls.
Lack of Pten in Fsp1-expressing CNS cells had a negligible impact on social and anxiety-like behaviors.

Conclusions:

The social and anxiety-like phenotypes associated with CNS-specific Pten deletion appear to depend on neuronal Pten.
Pten expression in Fsp1-positive cells (astrocytes) does not significantly contribute to these specific behaviors.
Further research is needed to elucidate the precise role of neuronal Pten in regulating social and anxiety behaviors.