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Impaired fear response in mice lacking GIT1.

Robert Schmalzigaug¹, Ramona M Rodriguiz, Pamela E Bonner

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

Neuroscience Letters

|April 23, 2009

Summary

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G protein-coupled receptor kinase interacting protein 1 (GIT1) knockout mice exhibit normal development but impaired fear responses. These findings highlight GIT1's role in amygdala-mediated emotional behaviors.

Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

G protein-coupled receptor kinase interacting protein 1 (GIT1) is an Arf GAP protein involved in neuronal functions.
GIT1 regulates processes like GPCR sequestration, cell migration, and synapse formation.

Purpose of the Study:

To investigate the in vivo function of GIT1 by generating and analyzing a global GIT1 knockout mouse model.
To assess the behavioral consequences of GIT1 deficiency in a whole-organism system.

Main Methods:

Generation of GIT1 knockout (GIT1-KO) mice using conditional Git1(flox) alleles and CMV-Cre transgene.
Behavioral analyses including exploratory, anxiety-like, depressive-like behaviors, fear conditioning, and fear-potentiated startle.

Main Results:

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GIT1-KO mice showed high mortality shortly after birth, but surviving adults were fertile and developed normally.
Adult GIT1-KO mice displayed normal exploratory, anxiety-, and depressive-like behaviors.
Significant impairments were observed in fear conditioning and fear-potentiated startle responses in GIT1-KO mice.

Conclusions:

GIT1 plays a crucial role in regulating amygdala-mediated, experience-based emotional behaviors.
The study establishes an in vivo model for GIT1 research, revealing its specific involvement in fear-related learning and memory.