CA1 pyramidal cell receptor dependent cAMP dynamics (Chay et al. 2016)

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Accession:184731
We use a combination of live cell imaging and stochastic modeling of signaling pathways to investigate how noradrenergic receptor stimulation interacts with calcium to control cAMP, required for synaptic plasticity and memory in the hippocampus. Our simulation results explain the mechanism whereby prior noradrenergic receptor stimulation does not enhance the subsequent NMDA stimulated cAMP elevation. Specifically, our results demonstrate the the negative feedback loop from cAMP, through PKA, to PDE4 cannot explain the results, and that switching of the noradrenergic receptor from Gs to Gi is required.
Reference:
1 . Chay A, Zamparo I, Koschinski A, Zaccolo M, Blackwell KT (2016) Control of ├čAR- and N-methyl-D-aspartate (NMDA) Receptor-Dependent cAMP Dynamics in Hippocampal Neurons. PLoS Comput Biol 12:e1004735 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Molecular Network;
Brain Region(s)/Organism:
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s):
Gap Junctions:
Receptor(s): NMDA; Adrenergic;
Gene(s):
Transmitter(s): Norephinephrine;
Simulation Environment: C or C++ program; Java; Python;
Model Concept(s): Synaptic Plasticity; Long-term Synaptic Plasticity; Signaling pathways; G-protein coupled; Reaction-diffusion;
Implementer(s): Blackwell, Avrama [avrama at gmu.edu];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; NMDA; Adrenergic; Norephinephrine;
 
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ChayEtAl2015
                            
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