Imperial College London
Alternate

ProfessorThomasBrand

Faculty of Medicine, National Heart & Lung Institute

Chair in Developmental Dynamics
 
 
 
//

Contact

 

+44 (0)20 7594 8744t.brand Website CV

 
 
//

Assistant

 

Miss Cheryl Costello +44 (0)20 7594 3001

 
//

Location

 

433ICTEM buildingHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@unpublished{Shetty:2021:10.1101/2021.05.12.443909,
author = {Shetty, MS and Ris, L and Schindler, RFR and Mizuno, K and Fedele, L and Giese, KP and Brand, T and Abel, T},
doi = {10.1101/2021.05.12.443909},
title = {Mice lacking the cAMP effector protein POPDC1 show enhanced hippocampal synaptic plasticity},
url = {http://dx.doi.org/10.1101/2021.05.12.443909},
year = {2021}
}
Download

RIS format (EndNote, RefMan)

TY  - UNPB
AB  - <jats:title>Abstract</jats:title><jats:p>Extensive research has uncovered diverse forms of synaptic plasticity and a wide array of molecular signaling mechanisms that act as positive or negative regulators. Specifically, cAMP-dependent signaling pathways have been crucially implicated in long-lasting synaptic plasticity. In this study, we examine the role of POPDC1 (or BVES), a cAMP effector protein expressed in brain, in modulating hippocampal synaptic plasticity. Unlike other cAMP effectors, such as PKA and EPAC, POPDC1 is membrane-bound and the sequence of the cAMP-binding cassette differs from canonical cAMP-binding domains. These properties suggest that POPDC1 may have a unique role in cAMP-mediated signaling underlying synaptic plasticity. Our results show that POPDC1 is enriched in hippocampal synaptoneurosomes. Acute hippocampal slices from <jats:italic>Popdc1</jats:italic> knockout (KO) mice exhibit enhanced long-term potentiation (LTP) induced by a variety of stimulation paradigms, particularly in response to weak stimulation paradigms that in slices from wildtype mice induce only transient LTP. Furthermore, <jats:italic>Popdc1</jats:italic> KO mice did not display any further enhancement in forskolin-induced LTP observed following inhibition of phosphodiesterases (PDEs), suggesting a possible modulation of cAMP-PDE signaling by POPDC1. Taken together, these data reveal POPDC1 as a novel player in the regulation of hippocampal synaptic plasticity and as a potential target for cognitive enhancement strategies.</jats:p>
AU  - Shetty,MS
AU  - Ris,L
AU  - Schindler,RFR
AU  - Mizuno,K
AU  - Fedele,L
AU  - Giese,KP
AU  - Brand,T
AU  - Abel,T
DO  - 10.1101/2021.05.12.443909
PY  - 2021///
TI  - Mice lacking the cAMP effector protein POPDC1 show enhanced hippocampal synaptic plasticity
UR  - http://dx.doi.org/10.1101/2021.05.12.443909
ER  -
Download