Effects of corticotropin releasing factor (CRF) on sleep and body temperature following controllable footshock stress in mice.
Summary of "Effects of corticotropin releasing factor (CRF) on sleep and body temperature following controllable footshock stress in mice."
Rapid eye movement sleep (REM) is increased after controllable stress (modeled by escapable footshock, ES) and decreased after uncontrollable stress (modeled by inescapable footshock, IS). Decreases in REM after IS are exacerbated by corticotropin releasing factor (CRF) and attenuated by a CRF antagonist. In this study, we trained mice with ES following injections of CRF, astressin (AST), or saline (SAL) to determine whether CRF would alter REM after ES. Male BALB/cJ mice (n=7) were implanted for recording sleep, activity and body temperature via telemetry and with a guide cannula aimed into a lateral ventricle. After recovery from surgery, sleep following exposure to a novel chamber was recorded as a handling control (HC). The mice received one day of training with ES without injection followed by weekly training sessions in which they received counterbalanced intracerebroventricular (ICV) microinjections of either SAL or CRF (days 7 & 14) or SAL or AST (days 21 & 28) prior to ES. On each experimental day, sleep was recorded for 20h. Compared to HC, the mice showed significantly increased REM when receiving either SAL or AST prior to ES whereas CRF prior to ES significantly reduced REM. Stress-induced hyperthermia had longer duration after ES compared to HC, and was not significantly altered by CRF or AST compared to SAL. The current results demonstrate that activity in the central CRF system is an important regulator of stress-induced alterations in REM.
Affiliation
Journal Details
This article was published in the following journal.
Name: Physiology & behavior
ISSN: 1873-507X
Pages: 886-92
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21651923
- DOI: http://dx.doi.org/10.1016/j.physbeh.2011.05.025
Medical and Biotech [MESH] Definitions
Receptors, Corticotropin-releasing Hormone
Cell surface proteins that bind corticotropin-releasing hormone with high affinity and trigger intracellular changes which influence the behavior of cells. The corticotropin releasing-hormone receptors on anterior pituitary cells mediate the stimulation of corticotropin release by hypothalamic corticotropin releasing factor. The physiological consequence of activating corticotropin-releasing hormone receptors on central neurons is not well understood.
Sleep Stages
Periods of sleep manifested by changes in EEG activity and certain behavioral correlates; includes Stage 1: sleep onset, drowsy sleep; Stage 2: light sleep; Stages 3 and 4: delta sleep, light sleep, deep sleep, telencephalic sleep.
Urocortins
Neuropeptides of about 40 amino acids which are structurally similar to CORTICOTROPIN-RELEASING FACTOR. Unlike CRF acting primarily through type 1 CRF RECEPTORS, urocortins signal preferentially through type 2 CRF receptors. Urocortins have wide tissue distribution from fish to mammals, and diverse functions. In mammals, urocortins can suppress food intake, delays gastric emptying, and decreases heat-induced edema.
Sleep Disorders, Intrinsic
Dyssomnias (i.e., insomnias or hypersomnias) associated with dysfunction of internal sleep mechanisms or secondary to a sleep-related medical disorder (e.g., sleep apnea, post-traumatic sleep disorders, etc.). (From Thorpy, Sleep Disorders Medicine, 1994, p187)
Parasomnias
Movements or behaviors associated with sleep, sleep stages, or partial arousals from sleep that may impair sleep maintenance. Parasomnias are generally divided into four groups: arousal disorders, sleep-wake transition disorders, parasomnias of REM sleep, and nonspecific parasomnias. (From Thorpy, Sleep Disorders Medicine, 1994, p191)
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