"Neurons use action potentials, or spikes, to encode information. Some neurons can store information for short periods (seconds to minutes) by continuing to spike after a stimulus ends, thus enabling working memory. This so-called “persistent” spiking occurs in many brain areas and has been linked to activation of canonical transient receptor potential (TRPC) channels. However, TRPC activation alone is insufficient to explain many aspects of persistent spiking such as resumption of spiking after periods of imposed quiescence. Using experiments and simulations, we show that calcium influx caused by spiking is necessary and sufficient to activate TRPC channels and that the ensuing positive feedback interaction between intracellular calcium and TRPC channel activation can account for many hitherto unexplained aspects of persistent spiking."
Model Type: Neuron or other electrically excitable cell
Currents: I CAN; I_AHP; I Na,t; I K
Model Concept(s): Calcium dynamics; Action Potentials; Working memory; Persistent activity
Simulation Environment: XPPAUT
Implementer(s): Prescott, Steven [steve.prescott at sickkids.ca]]
References:
Ratté S, Karnup S, Prescott SA. (2018). Nonlinear Relationship Between Spike-Dependent Calcium Influx and TRPC Channel Activation Enables Robust Persistent Spiking in Neurons of the Anterior Cingulate Cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience. 38 [PubMed]