Prefrontal cortex-dependent innate behaviors are altered by selective knockdown of Gad1 in neuropeptide Y interneurons

PloS One
Katelynn M CorderL E Dobrunz

Abstract

GABAergic dysfunction has been implicated in a variety of neurological and psychiatric disorders, including anxiety disorders. Anxiety disorders are the most common type of psychiatric disorder during adolescence. There is a deficiency of GABAergic transmission in anxiety, and enhancement of GABA transmission through pharmacological means reduces anxiety behaviors. GAD67-the enzyme responsible for GABA production-has been linked to anxiety disorders. One class of GABAergic interneurons, Neuropeptide Y (NPY) expressing cells, is abundantly found in brain regions associated with anxiety and fear learning, including prefrontal cortex, hippocampus and amygdala. Additionally, NPY itself has been shown to have anxiolytic effects, and loss of NPY+ interneurons enhances anxiety behaviors. A previous study showed that knockdown of Gad1 from NPY+ cells led to reduced anxiety behaviors in adult mice. However, the role of GABA release from NPY+ interneurons in adolescent anxiety is unclear. Here we used a transgenic mouse that reduces GAD67 in NPY+ cells (NPYGAD1-TG) through Gad1 knockdown and tested for effects on behavior in adolescent mice. Adolescent NPYGAD1-TG mice showed enhanced anxiety-like behavior and sex-dependent changes in loc...Continue Reading

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Citations

Apr 13, 2019·Autism Research : Official Journal of the International Society for Autism Research·Allison M J AnackerMichael D Saxe
May 8, 2020·Neurotoxicity Research·Fakhroddin AghajanpourAbdollah Amini
Feb 19, 2021·Brain Research·Allison AndersonKaroly Mirnics
Sep 22, 2021·Stress : the International Journal on the Biology of Stress·Mariana A CortesLynn E Dobrunz

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Methods Mentioned

BETA
transgenic
ELISA
dissection
Fluorescence
sedation

Software Mentioned

Prism
Med
Origin
Video Freeze
Image Studio Lite
SPSS Statistics

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