ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
Nonlinear Relationship Between Spike-Dependent Calcium Influx and TRPC Channel Activation Enables Robust Persistent Spiking in Neurons of the Anterior Cingulate Cortex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
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- A memristive circuit for self-organized network topology formation based on guided axon growth.Scientific reports · 2024Article
- Transient Receptor Potential Channels: Multiple Modulators of Peripheral Neuropathic Pain in Several Rodent Models.Neurochemical research · 2024Review
- Article
- TRPC4 and GIRK channels underlie neuronal coding of firing patterns that reflect GProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Activation of TRPC (Transient Receptor Potential Canonical) Channel Currents in Iron Overloaded Cardiac Myocytes.Circulation. Arrhythmia and electrophysiology · 2021Article
- Role of Transient Receptor Potential Canonical Channels in Heart Physiology and Pathophysiology.Frontiers in cardiovascular medicine · 2020Review
- Hydrogen Peroxide Gates a Voltage-Dependent Cation Current inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Continuation of spiking after a stimulus ends (i.e. persistent spiking) is thought to support working memory. Muscarinic receptor activation enables persistent spiking among synaptically isolated pyramidal neurons in anterior cingulate cortex (ACC), but a detailed characterization of that spiking is lacking and the underlying mechanisms remain unclear. Here, we show that the rate of persistent spiking in ACC neurons is insensitive to the intensity and number of triggers, but can be modulated by injected current, and that persistent spiking can resume after several seconds of hyperpolarization-imposed quiescence. Using electrophysiology and calcium imaging in brain slices from male rats, we determined that canonical transient receptor potential (TRPC) channels are necessary for persistent spiking and that TRPC-activating calcium enters in a spike-dependent manner via voltage-gated calcium channels. Constrained by these biophysical details, we built a computational model that reproduced the observed pattern of persistent spiking. Nonlinear dynamical analysis of that model revealed that TRPC channels become fully activated by the small rise in intracellular calcium caused by evoked spikes. Calcium continues to rise during persistent spiking, but because TRPC channel activation saturates, firing rate stabilizes. By calcium rising higher than required for maximal TRPC channel activation, TRPC channels are able to remain active during periods of hyperpolarization-imposed quiescence (until calcium drops below saturating levels) such that persistent spiking can resume when hyperpolarization is discontinued. Our results thus reveal that the robust intrinsic bistability exhibited by ACC neurons emerges from the nonlinear positive feedback relationship between spike-dependent calcium influx and TRPC channel activation.
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