The effects of galantamine and buspirone on sleep structure: Implications for understanding sleep abnormalities in major depression

Biard, Kathleen; Douglass, Alan B.; Koninck, Joseph De

doi:10.1177/0269881115598413

Cited by 20 publications

(13 citation statements)

References 32 publications

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“…The effects of the drugs on sleep structure are discussed more in depth in our previous article, 16 but it is worth noting here that both drugs affected sleep as predicted by current models of the serotonergic/cholinergic imbalance in depression. Our serotonergic agonist, buspirone, suppressed REM sleep by increasing RL.…”

Section: Discussionmentioning

confidence: 93%

“…The main effects of drug conditions across the entire sample of participants (ie, irrespective of genotype) are published elsewhere. 16 Averages and univariate results taking in account genotypes are presented in Table 1 . In brief, consistent with previous analyses, the mixed design repeated-measures MANOVA (with repeated measures across drug conditions and between measures of genotype groups) used in the present study revealed a significant effect of drug condition on sleep ( F =3.575, P <0.001).…”

Section: Resultsmentioning

confidence: 99%

“…Using pharmacological probes in healthy adults, we recently reported that a serotonergic agonist increases RL, while a promoter of cholinergic activity shortens RL and increases REM sleep duration. 16 These changes in REM sleep are well-aligned with the potential role of monoamine deregulation in the emergence of sleep disturbances in depression. Recent longitudinal studies have found that abnormal REM sleep measures such as shorter RL and elevated RD can predict the onset and course of depression in adolescents and adults.…”

Section: Introductionmentioning

confidence: 83%

“…Polysomnographic data for the entire sample of participants (irrespective of genotype) was previously published in a report on the effects of galantamine and buspirone on sleep. 16 …”

Section: Methodsmentioning

confidence: 99%

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A pilot study of serotonin-1A receptor genotypes and rapid eye movement sleep sensitivity to serotonergic/cholinergic imbalance in humans: a pharmacological model of depression

Biard

Douglass²,

Robillard

et al. 2015

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RationaleThe serotonergic and cholinergic systems are jointly involved in regulating sleep but this system is theorized to be disturbed in depressed individuals. We previously reported that cholinergic and serotonergic agents induce sleep changes partially consistent with monoamine models of sleep disturbances in depression. One potential cause of disturbed neurotransmission is genetic predisposition. The G(-1019) allele of the serotonin-1A (5-HT1A) receptor promoter region predicts an increased risk for depression compared to the wild-type C(-1019) allele.ObjectiveThe goal of this study was to investigate how serotonin-1A receptor genotypes mediate sleep sensitivity to pharmacological probes modeling the serotonergic/cholinergic imbalance of depression.MethodsSeventeen healthy female participants homozygous for either C (n=11) or G (n=6) alleles aged 18–27 years were tested on four nonconsecutive nights. Participants were given galantamine (an anti-acetylcholinesterase), buspirone (a serotonergic agonist), both drugs together, or placebos before sleeping.ResultsAs reported previously, buspirone significantly increased rapid eye movement (REM) latency (P<0.001), as well as awakenings, percentage of time spent awake, and percentage of time asleep spent in stage N1 (P<0.019). Galantamine increased awakenings, percentage of time spent awake, percentage of time asleep spent in stage N1, and percentage of time asleep spent in REM, and decreased REM latency and percentage of time asleep spent in stage N3 (P<0.019). Galantamine plus buspirone given together disrupted sleep more than either drug alone, lowering sleep efficiency and percentage of time asleep spent in stage N3 and increasing awakenings, percentage of time spent awake, and percentage of time asleep spent in stage N1 (P<0.019). There was no main effect of genotype nor was there a significant multivariate interaction between genotype and drug condition.ConclusionThese findings are partially consistent with the literature about sleep in depression, notably short REM latency, higher percentage of total sleep time spent in REM, lower percentage of time asleep spent in stage N3, and increased sleep fragmentation. The C/G mutation in the serotonin-1A receptor promoter region does not appear to cause noticeable differences in the sleep patterns of a relatively small sample of healthy young females. Future studies with larger sample sizes are required.

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Section: Discussionmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 83%

“…Polysomnographic data for the entire sample of participants (irrespective of genotype) was previously published in a report on the effects of galantamine and buspirone on sleep. 16 …”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

A pilot study of serotonin-1A receptor genotypes and rapid eye movement sleep sensitivity to serotonergic/cholinergic imbalance in humans: a pharmacological model of depression

Biard

Douglass²,

Robillard

et al. 2015

NSS

Self Cite

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show abstract

“…Nevertheless, this percentage increase in N3 sleep appears out of proportion to what has been reported in the literature. Our patient was also taking Bupropion (minimal effect on sleep architecture) [5], Venlafaxine (suppresses REM sleep and minimal effect on delta sleep) [6], Buspirone (decreases delta sleep) [7], and Methylphenidate (minimal effect on sleep architecture) [8] which are not known to increase stage N3 sleep.…”

Section: Introductionmentioning

confidence: 91%