ArticleFrontiers in computational neuroscience2014
The dendritic location of the L-type current and its deactivation by the somatic AHP current both contribute to firing bistability in motoneurons.
Article in Frontiers in computational neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Tonic Activation of Extrasynaptic NMDA Receptors Decreases Intrinsic Excitability and Promotes Bistability in a Model of Neuronal Activity.International journal of molecular sciences · 2019Article
- Curated Model Development Using NEUROiD: A Web-Based NEUROmotor Integration and Design Platform.Frontiers in neuroinformatics · 2019Article
- Contribution of intrinsic motoneuron properties to discharge hysteresis and its estimation based on paired motor unit recordings: a simulation study.Journal of neurophysiology · 2015Article
- Swimming against the tide: investigations of the C-bouton synapse.Frontiers in neural circuits · 2014Review
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3 authors at 2 institutions in 1 country.
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Abstract
Spinal motoneurons may display a variety of firing patterns including bistability between repetitive firing and quiescence and, more rarely, bistability between two firing states of different frequencies. It was suggested in the past that firing bistability required that the persistent L-type calcium current be segregated in distal dendrites, far away from the spike generating currents. However, this is not supported by more recent data. Using a two compartment model of motoneuron, we show that the different firing patterns may also result from the competition between the more proximal dendritic component of the dendritic L-type conductance and the calcium sensitive potassium conductance responsible for afterhypolarization (AHP). Further emphasizing this point, firing bistability may be also achieved when the L-type current is put in the somatic compartment. However, this requires that the calcium-sensitive potassium conductance be triggered solely by the high threshold calcium currents activated during spikes and not by calcium influx through the L-type current. This prediction was validated by dynamic clamp experiments in vivo in lumbar motoneurons of deeply anesthetized cats in which an artificial L-type current was added at the soma. Altogether, our results suggest that the dynamical interaction between the L-type and afterhyperpolarization currents is as fundamental as the segregation of the calcium L-type current in dendrites for controlling the discharge of motoneurons.
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