Modulation of burst frequency by calcium-dependent potassium channels in the lamprey locomotor system: Dependence of the activity level

Jesper Tegnér; Anders Lansner; Sten Grillner

doi:10.1023/A:1008897031013

Modulation of burst frequency by calcium-dependent potassium channels in the lamprey locomotor system: Dependence of the activity level

Jesper Tegnér^*, Anders Lansner, Sten Grillner

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

29 Scopus citations

Abstract

It is crucial to determine the effects on the network level of a modulation of intrinsic membrane properties. The role calcium-dependent potassium channels, K(Ca), in the lamprey locomotor system has been investigated extensively. Earlier experimental studies have shown that apamin, which affects one type of K(Ca), increases the cycle duration of the locomotor network, due to effects on the burst termination. The effects of apamin were here larger when the network had a low level of activity (burst frequency 0.5 to 1 Hz) as compared to a higher rate (> 2 Hz). By using a previously developed simulation model based on the lamprey locomotor network, we show that the model could account for the frequency dependence of the apamin modulation, if only the K(Ca) conductance activated by Ca²⁺ entering during the action potential was altered and not the K(Ca) conductance activated by Ca²⁺ entering through NMDA channels. The present simulation model of the spinal network in the lamprey can thus account for earlier experimental results with apamin on the network and cellular level that previously appeared enigmatic.

Original language	English (US)
Pages (from-to)	121-140
Number of pages	20
Journal	Journal of Computational Neuroscience
Volume	5
Issue number	2
DOIs	https://doi.org/10.1023/A:1008897031013
State	Published - 1998
Externally published	Yes

Bibliographical note

Funding Information:
We thank the reviewers and the action editor for their useful and thorough comments on this work. We are also indebted to Drs. Lennart Brodin, Abdel El-Manira, Russell Hill, David Parker, and Peter Wallén for valuable comments on the manuscript and Dr. Örjan Ekeberg for supplying the SWIM simulation software (see http://www.nada.kth.se/sans/). Patriq Fagerstedt provided useful help on the design of Figures 4 and 9. This work was supported by the Medical Research Council (Project No. 3026), the Swedish Natural Science Research Council (Project No. B-AA/BU03531), the Swedish National Board for Industrial and Technical Development, NUTEK (Project No. 8425-5-03075), and the Swedish Society for Medical Research.

Keywords

Computer simulation
K(Ca) channels
Modulation
Relaxation oscillator
Spinal circuits

ASJC Scopus subject areas

Sensory Systems
Cognitive Neuroscience
Cellular and Molecular Neuroscience

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10.1023/A:1008897031013

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title = "Modulation of burst frequency by calcium-dependent potassium channels in the lamprey locomotor system: Dependence of the activity level",

abstract = "It is crucial to determine the effects on the network level of a modulation of intrinsic membrane properties. The role calcium-dependent potassium channels, K(Ca), in the lamprey locomotor system has been investigated extensively. Earlier experimental studies have shown that apamin, which affects one type of K(Ca), increases the cycle duration of the locomotor network, due to effects on the burst termination. The effects of apamin were here larger when the network had a low level of activity (burst frequency 0.5 to 1 Hz) as compared to a higher rate (> 2 Hz). By using a previously developed simulation model based on the lamprey locomotor network, we show that the model could account for the frequency dependence of the apamin modulation, if only the K(Ca) conductance activated by Ca2+ entering during the action potential was altered and not the K(Ca) conductance activated by Ca2+ entering through NMDA channels. The present simulation model of the spinal network in the lamprey can thus account for earlier experimental results with apamin on the network and cellular level that previously appeared enigmatic.",

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author = "Jesper Tegn{\'e}r and Anders Lansner and Sten Grillner",

note = "Funding Information: We thank the reviewers and the action editor for their useful and thorough comments on this work. We are also indebted to Drs. Lennart Brodin, Abdel El-Manira, Russell Hill, David Parker, and Peter Wall{\'e}n for valuable comments on the manuscript and Dr. {\"O}rjan Ekeberg for supplying the SWIM simulation software (see http://www.nada.kth.se/sans/). Patriq Fagerstedt provided useful help on the design of Figures 4 and 9. This work was supported by the Medical Research Council (Project No. 3026), the Swedish Natural Science Research Council (Project No. B-AA/BU03531), the Swedish National Board for Industrial and Technical Development, NUTEK (Project No. 8425-5-03075), and the Swedish Society for Medical Research.",

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N1 - Funding Information: We thank the reviewers and the action editor for their useful and thorough comments on this work. We are also indebted to Drs. Lennart Brodin, Abdel El-Manira, Russell Hill, David Parker, and Peter Wallén for valuable comments on the manuscript and Dr. Örjan Ekeberg for supplying the SWIM simulation software (see http://www.nada.kth.se/sans/). Patriq Fagerstedt provided useful help on the design of Figures 4 and 9. This work was supported by the Medical Research Council (Project No. 3026), the Swedish Natural Science Research Council (Project No. B-AA/BU03531), the Swedish National Board for Industrial and Technical Development, NUTEK (Project No. 8425-5-03075), and the Swedish Society for Medical Research.

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N2 - It is crucial to determine the effects on the network level of a modulation of intrinsic membrane properties. The role calcium-dependent potassium channels, K(Ca), in the lamprey locomotor system has been investigated extensively. Earlier experimental studies have shown that apamin, which affects one type of K(Ca), increases the cycle duration of the locomotor network, due to effects on the burst termination. The effects of apamin were here larger when the network had a low level of activity (burst frequency 0.5 to 1 Hz) as compared to a higher rate (> 2 Hz). By using a previously developed simulation model based on the lamprey locomotor network, we show that the model could account for the frequency dependence of the apamin modulation, if only the K(Ca) conductance activated by Ca2+ entering during the action potential was altered and not the K(Ca) conductance activated by Ca2+ entering through NMDA channels. The present simulation model of the spinal network in the lamprey can thus account for earlier experimental results with apamin on the network and cellular level that previously appeared enigmatic.

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Modulation of burst frequency by calcium-dependent potassium channels in the lamprey locomotor system: Dependence of the activity level

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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