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


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.

Model Type: Molecular Network

Cell Type(s): Hippocampus CA1 pyramidal GLU cell

Receptors: NMDA; Adrenergic

Transmitters: Norephinephrine

Model Concept(s): Synaptic Plasticity; Long-term Synaptic Plasticity; Signaling pathways; G-protein coupled; Reaction-diffusion

Simulation Environment: C or C++ program; Java; Python

Implementer(s): Blackwell, Avrama [avrama at gmu.edu]

References:

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 computational biology. 12 [PubMed]


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