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   <subfield code="a">Cav2.3E-/R-type voltage-gated calcium channels modulate sleep in mice</subfield>
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   <subfield code="c">[A. Münch, M. Dibué, J. Hescheler, T. Schneider]</subfield>
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   <subfield code="a">Modulation des Schlafs durch spannungsgesteuerte Cav2.3-E- und Cav2.3-R-Typ-Kalziumkanäle in Mäusen</subfield>
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   <subfield code="a">Mammalian sleep is characterized by cycles of REM and non-REM (NREM), i.e. slow-wave sleep (SWS) phases. The major neuroanatomical basis of SWS is the thalamocortical circuitry, which operates in different functional modes to determine the state of vigilance. At high vigilance, the tonic mode predominates; stages of low vigilance and SWS are characterized by rebound burst firing. Electrophysiologically, rebound bursting depends on low-threshold Ca2 + spikes and T-type Ca2 + channels have been shown to modulate SWS. We recently demonstrated that Cav2.3R-type Ca2 + channels are capable of modulating absence seizures, a pathophysiological aberration of the thalamocortical oscillations related to SWS. We thus analyzed sleep architecture in control and Cav2.3(−|−) mice using implantable electroencephalography (EEG)/electromyography (EMG) radiotelemetry during spontaneous and urethane-induced sleep. The results demonstrate significantly reduced total sleep time and impairment of SWS generation in Cav2.3(−|−) mice, which affects global sleep architecture (i.e. the ratio of REM to NREM). Furthermore, the relative δ power is significantly reduced in Cav2.3(−|−) mice during NREM sleep although these mice display longer prior wakefulness, possibly indicating disturbances in sleep homeostasis. This observation is supported by recordings following urethane administration. This is the first study to shed light on the fundamental role of Cav2.3 channels in rodent sleep physiology.</subfield>
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