Similar effects were seen for mean REM sleep bout durations in the post-MD period ( Fig. 1C effects of treatment on % of total recording time for the three vigilance states: F = 6.3, p = 0.004 for NREM F = 7.1, p = 0.003 for REM H = 12.5, p = 0.006 for wake, one-way ANOVA). All three drugs led to significant decreases in rapid eye movement (REM) sleep, and concomitant increases in non-REM (NREM) sleep, relative to vehicle (VEH Fig. Polysomnography showed that the three hypnotics had similar effects on overall sleep/wake amounts and durations ( Fig. To investigate this possibility, we compared the effects of trazodone (TRA), zaleplon (ZAL) and eszopiclone (ESZ) on a classic in vivo form of cortical plasticity that is consolidated by sleep.Įffects of hypnotics on post-MD sleep architecture and EEG activity Because intracellular signaling pathways regulated by monoaminergic neurotransmission have been shown to modulate diverse forms of in vivo synaptic plasticity, , it is possible that antagonizing monoaminergic signaling with trazodone during sleep inhibits plasticity. In contrast to benzodiazepine and non-benzodiazepine hypnotics, the sedating antidepressant trazodone acts as both a weak serotonin (5-HT) reuptake inhibitor and as an antagonist at 5-HT 2A and 5-HT 2C, α 1-adrenergic, and histamine H 1 receptors. What has not been investigated, however, are the effects of other “z” hypnotics ( e.g., zaleplon, zopiclone), and the atypical, but commonly prescribed hypnotic trazodone on sleep-dependent brain plasticity. This suggests that certain classes of hypnotics targeting the GABA A receptor impair synaptic remodeling during sleep. We have previously shown that the effects of MD are consolidated by subsequent sleep, but inhibited by sleep deprivation, or when sleep is combined with the non-benzodiazepine hypnotic zolpidem –. Ocular dominance plasticity in the primary visual cortex (V1) is triggered by monocular deprivation (MD) during a critical developmental window. Importantly, the most commonly-prescribed hypnotics target diverse neurotransmitter systems that may interfere with plastic processes that occur during sleep. Certain hypnotic drugs can cause anterograde amnesia during wakefulness, , and may inhibit synaptic plasticity in vitro, , but it is unclear how they affect sleep-dependent consolidation processes and in vivo synaptic plasticity. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist.īehavioral findings in animals and humans suggest an important role for sleep in the consolidation of learning and memory however, much less is known about how sleep affects the synaptic and brain system-level changes that underlie these processes. and J.S., a L'Oréal USA For Women in Science fellowship to S.J.A., and a National Research Service Award from the National Eye Institute to S.J.A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: This work was supported by the University of Pennsylvania, Sepracor Pharmaceuticals, Pickwick postdoctoral fellowships from the National Sleep Foundation to S.J.A. Received: JanuAccepted: JPublished: July 1, 2009Ĭopyright: © 2009 Aton et al. PLoS ONE 4(7):Įditor: Olivier Jacques Manzoni, INSERM U862, France Citation: Aton SJ, Seibt J, Dumoulin MC, Coleman T, Shiraishi M, Frank MG (2009) The Sedating Antidepressant Trazodone Impairs Sleep-Dependent Cortical Plasticity.
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