N-type calcium channel α1B subunit (Cav2.2) Knock-out mice display hyperactivity and vigilance state differences

Carsten T. Beuckmann, Christopher M. Sinton, Norimasa Miyamoto, Mitsuhiro Ino, Masashi Yanagisawa

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Differential properties of voltage-dependent Ca2+ channels have been primarily ascribed to the α1 subunit, of which 10 different subtypes are currently known. For example, channels that conduct the N-type Ca2+ current possess the α1B subunit (Cav2.2), which has been localized, inter alia, to the piriform cortex, hippocampus, hypothalamus, locus coeruleus, dorsal raphe, thalamic nuclei, and granular layer of the cortex. Some of these regions have been previously implicated in metabolic and vigilance state control, and selective block of the N-type Ca2+ channel causes circadian rhythm disruption. In this study of Cav2.2-/- knock-out mice, we examined potential differences in feeding behavior, spontaneous locomotion, and the sleep-wake cyde. Cav2.2-/- mice did not display an overt metabolic phenotype but were hyperactive, demonstrating a 20% increase in activity under novel conditions and a 95% increase in activity under habituated conditions during the dark phase, compared with wild-type littermates. Cav2.2-/- mice also displayed vigilance state differences during the light phase, including increased consolidation of rapid-eye movement (REM) sleep and increased intervals between non-REM (NREM) and wakefulness episodes. EEG spectral power was increased during wakefulness and REM sleep and was decreased during NREM sleep in Cav2.2-/- mice. These results indicate a role of the N-type Ca2+ channel in activity and vigilance state control, which we interpret in terms of effects on neurotransmitter release.

Original languageEnglish (US)
Pages (from-to)6793-6797
Number of pages5
JournalJournal of Neuroscience
Volume23
Issue number17
StatePublished - Jul 30 2003

Fingerprint

N-Type Calcium Channels
Knockout Mice
Sleep
Wakefulness
REM Sleep
Thalamic Nuclei
Locus Coeruleus
Feeding Behavior
Locomotion
Eye Movements
Circadian Rhythm
Hypothalamus
Neurotransmitter Agents
Electroencephalography
Hippocampus
Phenotype
Light

Keywords

  • Calcium
  • EEG
  • Electroencephalogram
  • Locomotion
  • Mouse
  • REM sleep
  • Vigilance state

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

N-type calcium channel α1B subunit (Cav2.2) Knock-out mice display hyperactivity and vigilance state differences. / Beuckmann, Carsten T.; Sinton, Christopher M.; Miyamoto, Norimasa; Ino, Mitsuhiro; Yanagisawa, Masashi.

In: Journal of Neuroscience, Vol. 23, No. 17, 30.07.2003, p. 6793-6797.

Research output: Contribution to journalArticle

Beuckmann, Carsten T. ; Sinton, Christopher M. ; Miyamoto, Norimasa ; Ino, Mitsuhiro ; Yanagisawa, Masashi. / N-type calcium channel α1B subunit (Cav2.2) Knock-out mice display hyperactivity and vigilance state differences. In: Journal of Neuroscience. 2003 ; Vol. 23, No. 17. pp. 6793-6797.
@article{58b66a7ffdb94b7289f4149dc250b49f,
title = "N-type calcium channel α1B subunit (Cav2.2) Knock-out mice display hyperactivity and vigilance state differences",
abstract = "Differential properties of voltage-dependent Ca2+ channels have been primarily ascribed to the α1 subunit, of which 10 different subtypes are currently known. For example, channels that conduct the N-type Ca2+ current possess the α1B subunit (Cav2.2), which has been localized, inter alia, to the piriform cortex, hippocampus, hypothalamus, locus coeruleus, dorsal raphe, thalamic nuclei, and granular layer of the cortex. Some of these regions have been previously implicated in metabolic and vigilance state control, and selective block of the N-type Ca2+ channel causes circadian rhythm disruption. In this study of Cav2.2-/- knock-out mice, we examined potential differences in feeding behavior, spontaneous locomotion, and the sleep-wake cyde. Cav2.2-/- mice did not display an overt metabolic phenotype but were hyperactive, demonstrating a 20{\%} increase in activity under novel conditions and a 95{\%} increase in activity under habituated conditions during the dark phase, compared with wild-type littermates. Cav2.2-/- mice also displayed vigilance state differences during the light phase, including increased consolidation of rapid-eye movement (REM) sleep and increased intervals between non-REM (NREM) and wakefulness episodes. EEG spectral power was increased during wakefulness and REM sleep and was decreased during NREM sleep in Cav2.2-/- mice. These results indicate a role of the N-type Ca2+ channel in activity and vigilance state control, which we interpret in terms of effects on neurotransmitter release.",
keywords = "Calcium, EEG, Electroencephalogram, Locomotion, Mouse, REM sleep, Vigilance state",
author = "Beuckmann, {Carsten T.} and Sinton, {Christopher M.} and Norimasa Miyamoto and Mitsuhiro Ino and Masashi Yanagisawa",
year = "2003",
month = "7",
day = "30",
language = "English (US)",
volume = "23",
pages = "6793--6797",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "17",

}

TY - JOUR

T1 - N-type calcium channel α1B subunit (Cav2.2) Knock-out mice display hyperactivity and vigilance state differences

AU - Beuckmann, Carsten T.

AU - Sinton, Christopher M.

AU - Miyamoto, Norimasa

AU - Ino, Mitsuhiro

AU - Yanagisawa, Masashi

PY - 2003/7/30

Y1 - 2003/7/30

N2 - Differential properties of voltage-dependent Ca2+ channels have been primarily ascribed to the α1 subunit, of which 10 different subtypes are currently known. For example, channels that conduct the N-type Ca2+ current possess the α1B subunit (Cav2.2), which has been localized, inter alia, to the piriform cortex, hippocampus, hypothalamus, locus coeruleus, dorsal raphe, thalamic nuclei, and granular layer of the cortex. Some of these regions have been previously implicated in metabolic and vigilance state control, and selective block of the N-type Ca2+ channel causes circadian rhythm disruption. In this study of Cav2.2-/- knock-out mice, we examined potential differences in feeding behavior, spontaneous locomotion, and the sleep-wake cyde. Cav2.2-/- mice did not display an overt metabolic phenotype but were hyperactive, demonstrating a 20% increase in activity under novel conditions and a 95% increase in activity under habituated conditions during the dark phase, compared with wild-type littermates. Cav2.2-/- mice also displayed vigilance state differences during the light phase, including increased consolidation of rapid-eye movement (REM) sleep and increased intervals between non-REM (NREM) and wakefulness episodes. EEG spectral power was increased during wakefulness and REM sleep and was decreased during NREM sleep in Cav2.2-/- mice. These results indicate a role of the N-type Ca2+ channel in activity and vigilance state control, which we interpret in terms of effects on neurotransmitter release.

AB - Differential properties of voltage-dependent Ca2+ channels have been primarily ascribed to the α1 subunit, of which 10 different subtypes are currently known. For example, channels that conduct the N-type Ca2+ current possess the α1B subunit (Cav2.2), which has been localized, inter alia, to the piriform cortex, hippocampus, hypothalamus, locus coeruleus, dorsal raphe, thalamic nuclei, and granular layer of the cortex. Some of these regions have been previously implicated in metabolic and vigilance state control, and selective block of the N-type Ca2+ channel causes circadian rhythm disruption. In this study of Cav2.2-/- knock-out mice, we examined potential differences in feeding behavior, spontaneous locomotion, and the sleep-wake cyde. Cav2.2-/- mice did not display an overt metabolic phenotype but were hyperactive, demonstrating a 20% increase in activity under novel conditions and a 95% increase in activity under habituated conditions during the dark phase, compared with wild-type littermates. Cav2.2-/- mice also displayed vigilance state differences during the light phase, including increased consolidation of rapid-eye movement (REM) sleep and increased intervals between non-REM (NREM) and wakefulness episodes. EEG spectral power was increased during wakefulness and REM sleep and was decreased during NREM sleep in Cav2.2-/- mice. These results indicate a role of the N-type Ca2+ channel in activity and vigilance state control, which we interpret in terms of effects on neurotransmitter release.

KW - Calcium

KW - EEG

KW - Electroencephalogram

KW - Locomotion

KW - Mouse

KW - REM sleep

KW - Vigilance state

UR - http://www.scopus.com/inward/record.url?scp=0042133371&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0042133371&partnerID=8YFLogxK

M3 - Article

VL - 23

SP - 6793

EP - 6797

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

IS - 17

ER -