Forebrain elimination of cacna1c mediates anxiety-like behavior in mice
Autor: | Amy S. Lee, H De Jesus-Cortes, Aditi M Rajadhyaksha, Anjali M. Rajadhyaksha, Franz Hofmann, J K Britt, Anni S. Lee, Andrew A. Pieper, Keith L. Gonzales, Sven Moosmang, S Ra |
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Rok vydání: | 2012 |
Předmět: |
medicine.medical_specialty
Elevated plus maze Calcium Channels L-Type Prefrontal Cortex Striatum Anxiety Nucleus accumbens Open field Mice 03 medical and health sciences Cellular and Molecular Neuroscience Prosencephalon 0302 clinical medicine Internal medicine medicine Animals Maze Learning Prefrontal cortex Letter to the Editor Molecular Biology 030304 developmental biology Mice Knockout 0303 health sciences Ventral tegmental area Disease Models Animal Psychiatry and Mental health Endocrinology medicine.anatomical_structure Gene Knockdown Techniques Forebrain Psychology Neuroscience 030217 neurology & neurosurgery Basolateral amygdala |
Zdroj: | Molecular Psychiatry |
ISSN: | 1476-5578 1359-4184 |
DOI: | 10.1038/mp.2012.71 |
Popis: | The CACNA1C gene encoding the Cav1.2 subunit of the L-type calcium channel has emerged as a new candidate gene for neuropsychiatric disease, including bipolar disorder, major depression, schizophrenia and autism.1, 2, 3 We report that global haploinsufficiency, forebrain-specific elimination and prefrontal cortex (PFC)-specific knockdown of cacna1c all increase anxiety-related behavior in mice, a prominent component of the forms of neuropsychiatric disease in which aberrations in CACNA1C have been implicated, without affecting compulsive behavior. Constitutive cacna1c heterozygous mice (HET) were evaluated in three behavioral assays related to anxiety: open field test, light–dark conflict test and elevated plus maze (EPM). HETs displayed anxiety-like behavior in the EPM (Figure 1a), spending significantly less time exploring the open arms compared with wild-type littermate controls (WT; F1,19=6.437; P |
Databáze: | OpenAIRE |
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