Effects of eszopiclone and zolpidem on sleep–wake behavior, anxiety-like behavior and contextual memory in rats

Huang, Max P.; Radadia, Kushan; Macone, Brian W.; Auerbach, Sanford; Datta, Subimal

doi:10.1016/j.bbr.2010.02.018

Cited by 29 publications

(29 citation statements)

References 102 publications

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“…38-41 In addition, intraperitoneal administration of eszopiclone causes anxiolysis. 42 These findings fit with the concept that BZ site agonists produce their desired clinical actions by enhancing GABAergic inhibition, resulting in diminished neuronal excitability within the amygdala. This interpretative view of a mechanism of action of BZ site agonists also is consistent with the present finding that systemically administering midazolam and eszopiclone caused a significant decrease in ACh release in the amygdala of unanesthetized (Fig.…”

Section: Discussionsupporting

confidence: 70%

Benzodiazepine Site Agonists Differentially Alter Acetylcholine Release in Rat Amygdala

Hambrecht-Wiedbusch

Mitchell

Firn

et al. 2014

Anesthesia &Amp; Analgesia

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Background Agonist binding at the benzodiazepine site of γ-aminobutric acid type A receptors diminishes anxiety and insomnia by actions in the amygdala. The neurochemical effects of benzodiazepine-site agonists remain incompletely understood. Cholinergic neurotransmission modulates amygdala function, and in this study we tested the hypothesis that benzodiazepine-site agonists alter acetylcholine (ACh) release in the amygdala. Methods Microdialysis and high performance liquid chromatography quantified ACh release in the amygdala of Sprague-Dawley rats (n=33). ACh was measured before and after IV administration (3 mg/kg) of midazolam or eszopiclone, with and without anesthesia. ACh in isoflurane-anesthetized rats during dialysis with Ringer’s solution(control) was compared to ACh release during dialysis with Ringer’s solution containing (100 μM) midazolam, diazepam, eszopiclone, or zolpidem. Results In unanesthetized rats, ACh in the amygdala was decreased by IV midazolam (−51.1%; P=0.0029; 95% CI= −73.0% to −29.2%) and eszopiclone (−39.6%; P=0.0222; 95% CI= −69.8% to −9.3%). In anesthetized rats, ACh in the amygdala was decreased by IV administration of midazolam (−46.2%; P=0.0041; 95% CI= −67.9% to −24.5%) and eszopiclone (−34.0%; P=0.0009; 95% CI= −44.7% to −23.3%), and increased by amygdala delivery of diazepam (43.2%; P=0.0434; 95% CI= 2.1% to 84.3%), and eszopiclone (222.2%; P=0.0159; 95% CI= 68.5% to 375.8%). Conclusions ACh release in the amygdala was decreased by IV delivery of midazolam and eszopiclone. Dialysis delivery directly into the amygdala caused either increased (eszopiclone and diazepam) or likely no significant change (midazolam and zolpidem) in ACh release. These contrasting effects of delivery route on ACh release support the interpretation that systemically administered midazolam and eszopiclone decrease ACh release in the amygdala by acting on neuronal systems outside of the amygdala.

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Section: Discussionsupporting

confidence: 70%

Benzodiazepine Site Agonists Differentially Alter Acetylcholine Release in Rat Amygdala

Hambrecht-Wiedbusch

Mitchell

Firn

et al. 2014

Anesthesia &Amp; Analgesia

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“…Administration of the GABA B agonists sodium oxybate or baclofen before a nap increased SWS, without affecting sleep-dependent declarative memory consolidation of word pairs and face-location associations (1255). In rats, administration of the GABA A agonists eszopiclone and zolipem after learning before sleep impaired contextual memory tested 24 h later (577). Two more recent studies in humans showed similarly impairing effects of triazolam and zolpidem on sleep-dependent consolidation of finger sequence tapping skills (835,836).…”

Section: Gabamentioning

confidence: 95%

About Sleep's Role in Memory

Rasch

Born

2013

Physiological Reviews

2,234

2,026

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Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

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“…For power spectral analysis, cortical EEG signals were amplified and bandpass filtered (0.5 – 40 Hz) with a polygraph and Gamma software, as described previously [29, 30]. The amplified and filtered data was digitized at a sampling frequency of 256 Hz and subjected to a Fast Fourier transformation (0.5 – 40 Hz with an interval of 0.2 Hz; using SleepSign software) to calculate the cortical EEG power during the 6-h recording session (bin width of 5 second).…”

Section: Methodsmentioning

confidence: 99%

The homeostatic regulation of REM sleep: A role for localized expression of brain-derived neurotrophic factor in the brainstem

Datta

Knapp

Koul-Tiwari

et al. 2015

Behavioural Brain Research

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Homeostatic regulation of REM sleep plays a key role in neural plasticity and deficits in this process are implicated in the development of many neuropsychiatric disorders. Little is known, however, about the molecular mechanisms that underlie this homeostatic regulation process. This study examined the hypothesis that, during selective REM sleep deprivation (RSD), increased brain-derived neurotrophic factor (BDNF) expression in REM sleep regulating areas is critical for the development of homeostatic drive for REM sleep, as measured by an increase in the number of REM sleep transitions. Rats were assigned to RSD, non-sleep deprived (BSL), or total sleep deprivation (TSD) groups. Physiological recordings were obtained from cortical, hippocampal, and pontine EEG electrodes over a 6-hour period, in which sleep deprivation occurred during the first 3 hours. In the RSD, but not the other conditions, homeostatic drive for REM sleep increased progressively. BDNF protein expression was significantly greater in the pedunculopontine tegmentum (PPT) and subcoeruleus nucleus (SubCD) in the RSD as compared to the TSD and BSL groups, areas that regulate REM sleep, but not in the medial preoptic area, which regulates non-REM sleep. There was a significant positive correlation between RSD-induced increases in number of REM sleep episodes and increased BDNF expression in the PPT and SubCD. These increases positively correlated with levels of homeostatic drive for REM sleep. These results, for the first time, suggest that selective RSD-induced increased expression of BDNF in the PPT and SubCD are determinant factors in the development of the homeostatic drive for REM sleep.

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Effects of eszopiclone and zolpidem on sleep–wake behavior, anxiety-like behavior and contextual memory in rats

Cited by 29 publications

References 102 publications

Benzodiazepine Site Agonists Differentially Alter Acetylcholine Release in Rat Amygdala

Benzodiazepine Site Agonists Differentially Alter Acetylcholine Release in Rat Amygdala

About Sleep's Role in Memory

The homeostatic regulation of REM sleep: A role for localized expression of brain-derived neurotrophic factor in the brainstem

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