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Deletion of Gαq in the telencephalon alters specific neurobehavioral outcomes.

Title: Deletion of Gαq in the telencephalon alters specific neurobehavioral outcomes.
Name(s): Graham, Devon L, author
Buendia, Matthew A, author
Chapman, Michelle A, author
Durai, Heather H, author
Stanwood, Gregg D, author
Type of Resource: text
Genre: Journal Article
Date Issued: 2015-09-01
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: G(αq) -coupled receptors are ubiquitously expressed throughout the brain and body, and it has been shown that these receptors and associated signaling cascades are involved in a number of functional outputs, including motor function and learning and memory. Genetic alterations to G(αq) have been implicated in neurodevelopmental disorders such as Sturge-Weber syndrome. Some of these associated disease outcomes have been modeled in laboratory animals, but as G(αq) is expressed in all cell types, it is difficult to differentiate the underlying circuitry or causative neuronal population. To begin to address neuronal cell type diversity in G(αq) function, we utilized a conditional knockout mouse whereby G(αq) was eliminated from telencephalic glutamatergic neurons. Unlike the global G(αq) knockout mouse, we found that these conditional knockout mice were not physically different from control mice, nor did they exhibit any gross motor abnormalities. However, similarly to the constitutive knockout animal, G(αq) conditional knockout mice demonstrated apparent deficits in spatial working memory. Loss of G(αq) from glutamatergic neurons also produced enhanced sensitivity to cocaine-induced locomotion, suggesting that cortical G(αq) signaling may limit behavioral responses to psychostimulants. Screening for a variety of markers of forebrain neuronal architecture revealed no obvious differences in the conditional knockouts, suggesting that the loss of G(αq) in telencephalic excitatory neurons does not result in major alterations in brain structure or neuronal differentiation. Taken together, our results define specific modulation of spatial working memory and psychostimulant responses through disruptions in G(αq) signaling within cerebral cortical glutamatergic neurons.
Identifier: FSU_pmch_25963901 (IID), 10.1002/syn.21830 (DOI), PMC4514547 (PMCID), 25963901 (RID), 25963901 (EID)
Keywords: Emx1, Gnaq, Anxiety, Conditional knockout, Glutamate, Locomotor activity, Spatial working memory
Grant Number: P30 HD015052, R01 MH086629, P30HD15052, R01MH086629
Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at
Subject(s): Animals
Dopamine Uptake Inhibitors/pharmacology
GTP-Binding Protein alpha Subunits, Gq-G11/deficiency
GTP-Binding Protein alpha Subunits, Gq-G11/genetics
Glutamic Acid/metabolism
Mice, Inbred C57BL
Mice, Knockout
Motor Activity/drug effects
Motor Activity/physiology
Neurons/drug effects
Telencephalon/drug effects
Persistent Link to This Record:
Owner Institution: FSU
Is Part Of: Synapse (New York, N.Y.).
Issue: iss. 9, vol. 69

Choose the citation style.
Graham, D. L., Buendia, M. A., Chapman, M. A., Durai, H. H., & Stanwood, G. D. (2015). Deletion of Gαq in the telencephalon alters specific neurobehavioral outcomes. Synapse (New York, N.y.). Retrieved from