Sleep and EEG power spectrum effects of the 5-HT1A antagonist NAN-190 alone and in combination with citalopram

The sleep and waking and EEG power spectrum effects of the putative 5-HT1A antagonist NAN-190 (0.5 mg/kg, i.p.) were studied alone and in co-administration with the selective serotonin re-uptake inhibitor citalopram (5.0 mg/kg, i.p.) in the rat. Citalopram, as in a prior dose-response study, reduced...

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Bibliographic Details
Published in:Behavioural brain research 1996-02, Vol.75 (1-2), p.159-168
Main Authors: Neckelmann, D, Bjørkum, A A, Bjorvatn, B, Ursin, R
Format: Article
Language:English
Subjects:
Animals
Behavior, Animal - drug effects
Citalopram - pharmacology
Drug Interactions
Electroencephalography - drug effects
Male
Piperazines - pharmacology
Rats
Rats, Wistar
Serotonin Antagonists - pharmacology
Serotonin Uptake Inhibitors - pharmacology
Sleep - drug effects
Sleep Stages - drug effects
Sleep, REM - drug effects
Synapses - drug effects
Synapses - metabolism
Wakefulness - drug effects
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Summary:The sleep and waking and EEG power spectrum effects of the putative 5-HT1A antagonist NAN-190 (0.5 mg/kg, i.p.) were studied alone and in co-administration with the selective serotonin re-uptake inhibitor citalopram (5.0 mg/kg, i.p.) in the rat. Citalopram, as in a prior dose-response study, reduced REM sleep. In addition, a slight increase in NREM sleep was observed. Citalopram reduced NREM fronto-parietal (FP) EEG power density in the 5-20 Hz range. When administered alone, NAN-190 suppressed REM sleep in the first 2 h, and reduced SWS-2 in the first 4 after administration. NAN-190 also suppressed selectively NREM sleep slow-wave activity in both fronto-frontal (FF) and FP EEG power spectrum. When administered in combination with citalopram, an attenuation of the power density reduction in the 7-15 Hz range in the FF EEG of citalopram alone, was observed. However, the EEG power spectral density and REM sleep suppressive effects of NAN-190 were both augmented. The results are compatible with the notion that serotonin is involved in the modulation of the slow wave activity in the EEG during NREM sleep. The results are cordant with other data suggesting that postsynaptic 5-HT1A stimulation might increase slow wave activity in the NREM EEG, and that serotonergic stimulation of other receptor subtypes (possibly 5-HT2) may decrease slow wave activity in the NREM EEG.
ISSN:0166-4328
DOI:10.1016/0166-4328(96)00204-5