ArticleThe Journal of physiology2011
Distinct roles for I(T) and I(H) in controlling the frequency and timing of rebound spike responses.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- 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
- Article
- A small, computationally flexible network produces the phenotypic diversity of song recognition in crickets.eLife · 2021Article
- Modeling temperature- and Cav3 subtype-dependent alterations in T-type calcium channel mediated burst firing.Molecular brain · 2021Article
- Homeostatic plasticity and burst activity are mediated by hyperpolarization-activated cation currents and T-type calcium channels in neuronal cultures.Scientific reports · 2021Article
- Electrophysiological and Morphological Features of Rebound Depolarization Characterized Interneurons in Rat Superficial Spinal Dorsal Horn.Frontiers in cellular neuroscience · 2021Article
- Developmental Changes in Serotonergic Modulation of GABAergic Synaptic Transmission and Postsynaptic GABACerebellum (London, England) · 2018Article
- Dynamical Mechanism of Hyperpolarization-Activated Non-specific Cation Current Induced Resonance and Spike-Timing Precision in a Neuronal Model.Frontiers in cellular neuroscience · 2018Article
- Phasic inhibition as a mechanism for generation of rapid respiratory rhythms.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Down-regulation of T-type Cav3.2 channels by hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1): Evidence of a signaling complex.Channels (Austin, Tex.) · 2017Article
- Serotonin modulates response properties of neurons in the dorsal cochlear nucleus of the mouse.Hearing research · 2017Article
- Synchronicity and Rhythmicity of Purkinje Cell Firing during Generalized Spike-and-Wave Discharges in a Natural Mouse Model of Absence Epilepsy.Frontiers in cellular neuroscience · 2017Article
- Inhibition promotes long-term potentiation at cerebellar excitatory synapses.Scientific reports · 2016Article
- Determinants of rebound burst responses in rat cerebellar nuclear neurons to physiological stimuli.The Journal of physiology · 2016Article
- Whole-Cell Properties of Cerebellar Nuclei Neurons In Vivo.PloS one · 2016Article
- A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia.American journal of human genetics · 2015Article
- Characterisation of rebound depolarisation in mice deep dorsal horn neurons in vitro.Pflugers Archiv : European journal of physiology · 2015Article
- PKA reduces the rat and human KCa3.1 current, CaM binding, and Ca2+ signaling, which requires Ser332/334 in the CaM-binding C terminus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- T-type channels buddy up.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
The ability for neurons to generate rebound bursts following inhibitory synaptic input relies on ion channels that respond in a unique fashion to hyperpolarization. Inward currents provided by T-type calcium channels (I(T)) and hyperpolarization-activated HCN channels (I(H)) increase in availability upon hyperpolarization, allowing for a rebound depolarization after a period of inhibition. Although rebound responses have long been recognized in deep cerebellar nuclear (DCN) neurons, the actual extent to which I(T) and I(H) contribute to rebound spike output following physiological levels of membrane hyperpolarization has not been clearly established. The current study used recordings and simulations of large diameter cells of the in vitro rat DCN slice preparation to define the roles for I(T) and I(H) in a rebound response. We find that physiological levels of hyperpolarization make only small proportions of the total I(T) and I(H) available, but that these are sufficient to make substantial contributions to a rebound response. At least 50% of the early phase of the rebound spike frequency increase is generated by an I(T)-mediated depolarization. An additional frequency increase is provided by I(H) in reducing the time constant and thus the extent of I(T) inactivation as the membrane returns from a hyperpolarized state to the resting level. An I(H)-mediated depolarization creates an inverse voltage-first spike latency relationship and produces a 35% increase in the precision of the first spike latency of a rebound. I(T) and I(H) can thus be activated by physiologically relevant stimuli and have distinct roles in the frequency, timing and precision of rebound responses.
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