ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Local control of postinhibitory rebound spiking in CA1 pyramidal neuron dendrites.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Transient boosting of action potential backpropagation for few-shot temporal pattern learning.PLoS computational biology · 2025Article
- Characterizing optogenetically mediated rebound effects in anaesthetized mouse primary visual cortex.The Journal of physiology · 2025Article
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- Interleaved single and bursting spiking resonance in neurons.PLoS computational biology · 2025Article
- Community-based reconstruction and simulation of a full-scale model of the rat hippocampus CA1 region.PLoS biology · 2024Article
- Variable recruitment of distal tuft dendrites shapes new hippocampal place fields.bioRxiv : the preprint server for biology · 2024Article
- The neuronal and synaptic dynamics underlying post-inhibitory rebound burst related to major depressive disorder in the lateral habenula neuron model.Cognitive neurodynamics · 2024Article
- Conditioning and pseudoconditioning differently change intrinsic excitability of inhibitory interneurons in the neocortex.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- An Adaptive Generalized Leaky Integrate-and-Fire Model for Hippocampal CA1 Pyramidal Neurons and Interneurons.Bulletin of mathematical biology · 2023Article
- Simulations predict differing phase responses to excitation vs. inhibition in theta-resonant pyramidal neurons.Journal of neurophysiology · 2023Article
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- Single Neuron Modeling Identifies Potassium Channel Modulation as Potential Target for Repetitive Head Impacts.Neuroinformatics · 2023Article
- Geometric characterization of dynamical structure for neural firing activities induced by inhibitory pulse.Cognitive neurodynamics · 2022Article
- Assessing Local and Branch-specific Activity in Dendrites.Neuroscience · 2022Article
- Altered neocortical oscillations and cellular excitability in an in vitro Wwox knockout mouse model of epileptic encephalopathy.Neurobiology of disease · 2021Article
- IProgress in biophysics and molecular biology · 2021Review
- Modeling Neurotransmission: Computational Tools to Investigate Neurological Disorders.International journal of molecular sciences · 2021Review
- Modeling Reveals Human-Rodent Differences in H-Current Kinetics Influencing Resonance in Cortical Layer 5 Neurons.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- A Hypothesis for Theta Rhythm Frequency Control in CA1 Microcircuits.Frontiers in neural circuits · 2021Article
- Illuminating dendritic function with computational models.Nature reviews. Neuroscience · 2020Review
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4 authors.
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Abstract
Postinhibitory rebound spiking is characteristic of several neuron types and brain regions, where it sustains spontaneous activity and central pattern generation. However, rebound spikes are rarely observed in the principal cells of the hippocampus under physiological conditions. We report that CA1 pyramidal neurons support rebound spikes mediated by hyperpolarization-activated inward current (I(h)), and normally masked by A-type potassium channels (K(A)). In both experiments and computational models, K(A) blockage or reduction consistently resulted in a somatic action potential upon release from hyperpolarizing injections in the soma or main apical dendrite. Rebound spiking was systematically abolished by the additional blockage or reduction of I(h). Since the density of both K(A) and I(h) increases in these cells with the distance from the soma, such "latent" mechanism may be most effective in the distal dendrites, which are targeted by a variety of GABAergic interneurons. Detailed computer simulations, validated against the experimental data, demonstrate that rebound spiking can result from activation of distal inhibitory synapses. In particular, partial K(A) reduction confined to one or few branches of the apical tuft may be sufficient to elicit a local spike following a train of synaptic inhibition. Moreover, the spatial extent and amount of K(A) reduction determines whether the dendritic spike propagates to the soma. These data suggest that the plastic regulation of K(A) can provide a dynamic switch to unmask postinhibitory spiking in CA1 pyramidal neurons. This newly discovered local modulation of postinhibitory spiking further increases the signal processing power of the CA1 synaptic microcircuitry.
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