Abstract
The cAMP-dependent protein kinase (PKA) Cβ gene encodes three isoforms, two of which (Cβ2 and Cβ3) are transcribed from neural-specific promoters. Here we report the effects of knocking out all PKA Cβ subunit isoforms in mice. Total PKA activity was unaffected in the hippocampus and amygdala, while basal PKA activity was reduced by 26% in the brains of Cβall −/− mice despite a compensatory increase in Cα protein. Cued fear conditioning was disrupted in Cβall −/− mice when tested on a mixed C57BL/6/129 background but was indistinguishable from wild type mice when bred onto a 98% C57BL/6 background. This suggests an amygdala-specific deficit in the Cβall null mice that is sensitive to strain-specific genetic modifiers. Behavioral testing including locomotor activity, contextual fear conditioning, and conditioned taste aversion was normal in Cβall null mice on the 50% C57BL/6J background. We conclude that Cβ protein is not essential for neuronal development or function but may play a more subtle role in memory that is modulated by strain-specific genetic modifiers.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
