Different types of avoidance behavior in rats produce dissociable post-training changes in sleep

Fogel, Stuart; Smith, Carlyle; Higginson, Caitlin; Beninger, Richard J.

doi:10.1016/j.physbeh.2010.10.024

Cited by 13 publications

(8 citation statements)

References 33 publications

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“…The loss of sleep and increase in W demonstrated on these 2 days are typical characteristics of anxiety in both humans and animals (Monti and Monti, 2000; Lavie, 2001; Ohayon and Roth, 2003; Maclean and Datta, 2007; Pawlyk et al, 2008; Sanford and Yang, 2010; Macone et al, 2011; Yang et al, 2011). Contrary to the results of the present study, the previous studies that examined S-W changes associated with the LH model showed that SWS increases after the first day of LH training (Adrien et al, 1991; Fogel et al, 2011). This discrepancy could be explained by the fact that, as explained in the Introduction, these two prior studies incorporated learning components, and learning and memory has been shown to increase sleep (Karni et al, 1994; Smith, 1995; Stickgold et al, 2000; Walker et al, 2002; Huber et al, 2004).…”

Section: Discussioncontrasting

confidence: 99%

“…Numerous studies have utilized repetitive inescapable foot-shock as an AS to induce depression using a range of number, duration, and intensity of foot-shocks. Thus, in the present study, the chosen foot-shock parameters were strong enough to induce depression and a reversible depression-associated S-W phenotype, but not so strong that they bordered on any ethical boundaries, which have become increasingly stringent in recent years, as occurs in LH studies (Adrien et al, 1991; Fogel et al, 2011). Additionally, experimental testing was conducted in adult rats, which drastically reduced total experimental duration, compared to some of the aforementioned animal models of depression.…”

Section: Introductionmentioning

confidence: 76%

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Effect of Five-Consecutive-Day Exposure to an Anxiogenic Stressor on Sleep-Wake Activity in Rats

O’Malley¹,

Fishman²,

Ciraulo³

et al. 2013

Front. Neurol.

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Repeated exposure to an anxiogenic stressor (AS) is a known environmental factor for the development of depression, yet the progression of sleep-wake (S-W) changes associated with the onset of AS-induced depression (ASID) is not completely understood. Thus, the aim of this study was to identify these progressive S-W changes by developing ASID in rats, via repeated exposure to an AS, and compare this ASID-associated sleep phenotype with the sleep phenotype of human depression. To achieve this aim, rats were first recorded for a 6 h period of baseline S-W activity without AS. Then, rats were subjected to 5 days of AS [Day 1: inescapable foot-shock; 5 trials of 3 s foot-shocks (1.0 mA) at 3 min intervals; Days 3–5: 15 trials of 5 s foot-shocks at 45 s intervals]. S-W activity was recorded for 6 h immediately after each AS treatment session. Two days later rats were again recorded for 6 h of S-W activity, but with no exposure to the AS (NASD). Compared to the baseline day: Day 1 of AS (ASD-1) increased wakefulness, slow-wave sleep (SWS) latency, and rapid-eye movement (REM) sleep latency, but decreased the total amount of REM sleep; ASD-2 animals remained awake throughout the 6 h S-W recording period; ASD-3, ASD-4, and ASD-5 (ASDs-3–5) decreased wakefulness, SWS latency, and REM sleep latency, but increased the total amount of REM sleep. Interestingly, these results reveal that initial exposure to the AS versus later, repeated exposure to the AS produced opposing S-W changes. On NASD, animals exhibited baseline-like S-W activity, except slightly less REM sleep. These results suggest that repeated AS produces a sleep phenotype that resembles the sleep phenotype of depression in humans, but consistent re-exposure to the AS is required. These results are promising because the methodological simplicity and reversibility of the ASID-associated S-W phenotype could be more advantageous than other animal models for studying the pathophysiological mechanisms that underlie the expression of ASID.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 76%

Effect of Five-Consecutive-Day Exposure to an Anxiogenic Stressor on Sleep-Wake Activity in Rats

O’Malley¹,

Fishman²,

Ciraulo³

et al. 2013

Front. Neurol.

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“…; Fogel et al . ). A second, well‐characterized oscillator reliant upon voltage‐gated Ca 2+ channels is in the catecholamine secreting adrenal chromaffin cell in which there is an interplay between Ca V 1.3 channels and Ca 2+ ‐activated K + channels (BK, SK).…”

Section: Primary Hyperaldosteronismmentioning

confidence: 97%

“…These so-called pacemaker channel conductances often rely on voltage-gated Ca 2+ channels to produce the large, rising phase that characterizes the depolarizing component of the voltage oscillation. For example, a well-characterized oscillator reliant upon T-type Ca 2+ channels is found in thalamocortical neurons of the thalamus, in which an interplay between T-type Ca 2+ channels and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels drives voltage oscillations likely to be important for memory consolidation during sleep (Gais et al 2002;Eschenko et al 2006;Fogel et al 2011). A second, well-characterized oscillator reliant upon voltage-gated Ca 2+ channels is in the catecholamine secreting adrenal chromaffin cell in which there is an interplay between Ca V 1.3 channels and Ca 2+ -activated K + channels (BK, SK).…”

Section: Pacemakers In the Zona Glomerulosamentioning

confidence: 99%

Role of voltage‐gated calcium channels in the regulation of aldosterone production from zona glomerulosa cells of the adrenal cortex

Barrett

Guagliardo

Klein

et al. 2016

The Journal of Physiology

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Zona glomerulosa cells (ZG) of the adrenal gland constantly integrate fluctuating ionic, hormonal and paracrine signals to control the synthesis and secretion of aldosterone. These signals modulate Ca levels, which provide the critical second messenger to drive steroid hormone production. Angiotensin II is a hormone known to modulate the activity of voltage-dependent L- and T-type Ca channels that are expressed on the plasma membrane of ZG cells in many species. Because the ZG cell maintains a resting membrane voltage of approximately -85 mV and has been considered electrically silent, low voltage-activated T-type Ca channels are assumed to provide the primary Ca signal that drives aldosterone production. However, this view has recently been challenged by human genetic studies identifying somatic gain-of-function mutations in L-type Ca 1.3 channels in aldosterone-producing adenomas of patients with primary hyperaldosteronism. We provide a review of these assumptions and challenges, and update our understanding of the state of the ZG cell in a layer in which native cellular associations are preserved. This updated view of Ca signalling in ZG cells provides a unifying mechanism that explains how transiently activating Ca 3.2 channels can generate a significant and recurring Ca signal, and how Ca 1.3 channels may contribute to the Ca signal that drives aldosterone production.

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“…Alternatively, REM sleep is increased following safety conditioning (where animals learn that they will not be exposed to aversive stimuli in a given environment or given a specific cue never paired with the aversive stimulus) (76) or shuttle-box avoidance training (where the animals learn that they can terminate the unconditioned stimulus by escaping to a different compartment of the training cage (67–77). Depriving rats of REM sleep before conditioning impairs both cued and contextual fear conditioning, as well as learning and recall on a discriminative avoidance task (78, 79).…”

Section: Sleep-dependent Emotion and Memory Processes: Animal And Hummentioning

confidence: 99%

Sleep Disturbances as the Hallmark of PTSD: Where Are We Now?

Germain

2013

AJP

511

379

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The hypothesis that rapid eye movement (REM) sleep disturbances are the hallmark of posttraumatic stress disorder (PTSD), proposed by Ross and colleagues in 1989, has stimulated a wealth of clinical, preclinical, and animal studies on the role of sleep in the pathophysiology of PTSD. The present review revisits this influential hypothesis in light of clinical and experimental findings that have since accumulated. Polysomnographic studies conducted in adults with PTSD have yielded mixed findings regarding REM sleep disturbances, and they generally suggest modest and nonspecific sleep disruptions. Prospective and treatment studies have provided more robust evidence for the relationship between sleep disturbances and psychiatric outcomes and symptoms. Experimental animal and human studies that have probed the relationship between REM sleep and fear responses, as well as studies focused more broadly on sleep-dependent affective and memory processes, also provide strong support for the hypothesis that sleep plays an important role in PTSD-relevant processes. Overall, the literature suggests that disturbed REM or non-REM sleep can contribute to maladaptive stress and trauma responses and may constitute a modifiable risk factor for poor psychiatric outcomes. Clinicians need to consider that the chronic sleep disruption associated with nightmares may affect the efficacy of first-line PTSD treatments, but targeted sleep treatments may accelerate recovery from PTSD. The field is ripe for prospective and longitudinal studies in high-risk groups to clarify how changes in sleep physiology and neurobiology contribute to increased risk of poor psychiatric outcomes.

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Different types of avoidance behavior in rats produce dissociable post-training changes in sleep

Cited by 13 publications

References 33 publications

Effect of Five-Consecutive-Day Exposure to an Anxiogenic Stressor on Sleep-Wake Activity in Rats

Effect of Five-Consecutive-Day Exposure to an Anxiogenic Stressor on Sleep-Wake Activity in Rats

Role of voltage‐gated calcium channels in the regulation of aldosterone production from zona glomerulosa cells of the adrenal cortex

Sleep Disturbances as the Hallmark of PTSD: Where Are We Now?

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