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Anxiety-like behaviors in mice lacking GIT2.

Robert Schmalzigaug¹, Ramona M Rodriguiz, Lindsey E Phillips

¹Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.

Neuroscience Letters

|December 31, 2008

Summary

G protein-coupled receptor kinase-interactor 2 (GIT2) knockout mice exhibit anxiety-like behaviors. These GIT2-deficient mice show no signs of depression, suggesting a specific role for GIT2 in mood regulation.

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Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

G protein-coupled receptor kinase-interactor 2 (GIT2) is a signaling scaffold protein and GTPase-activating protein (GAP) for ADP-ribosylation factor (Arf) small GTP-binding proteins.
GIT2 plays roles in G protein-coupled receptor trafficking, cell adhesion, and migration.

Purpose of the Study:

To investigate the in vivo neurobehavioral functions of GIT2.
To evaluate potential abnormalities in emotionality and mood in GIT2-knockout (KO) mice.

Main Methods:

Generation and behavioral assessment of GIT2-knockout (KO) mice.
Utilized behavioral tests including the zero-maze, light-dark emergence test, and tail suspension test.

Main Results:

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Both male and female GIT2-KO mice displayed anxiety-like behaviors in the zero-maze and light-dark emergence tests.
GIT2-KO males showed reduced immobility in the tail suspension test, indicative of antidepressant-like effects, while females did not.
Overall, GIT2-KO mice exhibit anxiety-like behavior without accompanying depressive-like responses.

Conclusions:

GIT2 plays a significant role in regulating anxiety-like behaviors.
The absence of GIT2 leads to specific neurobehavioral alterations, particularly anxiety, without a general depressive phenotype.