Comprehensive Physiology Wiley Online Library

Hormones, Cytokines, and Sleep

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Abstract

The sections in this article are:

1 Sleep‐Related Hormone Changes
2 Rhythms of Hormones
2.1 The Somatotropic Axis
2.2 Corticotropin‐Glucocorticoid Axis
2.3 Thyroid‐Stimulating Hormone‐Thyroid Axis
2.4 The Gonadotropins‐gonad Axis
2.5 Prolactin
2.6 Melatonin
2.7 Renin (Angiotensin)‐Aldosterone System
2.8 Other Hormones
3 Effects of Hormones on Sleep
3.1 Somatotropic Axis
3.2 Corticotropin‐Releasing Hormone‐Corticotropin Axis
3.3 Thyroid Hormones
3.4 Gonadotropins
3.5 Prolactin and Vasoactive Intestinal Peptide
3.6 Vasopressin
3.7 Steroid Hormones
3.8 Melatonin
3.9 Gastrointestinal Hormones
4 Cytokines
5 Infection and Sleep
6 Effects of Cytokines on Sleep
6.1 Interleukin‐1
6.2 Tumor Necrosis Factor
6.3 Interferons
6.4 Fibroblast Growth Factor
6.5 IL‐10, IL‐2, and IL‐6
7 Links Between the Effects of Cytokines and Hormones on Sleep
8 Conclusion
Figure 1. Figure 1.

The diurnal rhythms of hypothalamic growth hormone‐releasing hormone (GHRH) content, GHRH mRNA expression, and the duration of nonrapid eye movement sleep (NREMS) in rats. Measurements obtained in groups of rats sacrificed or recorded in various time points are double‐plotted for two consecutive 24‐h days each consisting of a 12‐h light and a 12‐h dark period. Time 0 and Time 24 indicate the onset of the light periods. Dark periods are marked by horizontal black bars.

Figure 2. Figure 2.

Effects of systemic injection of GHRH (0.5 g/kg) on sleep in intact and hypophysectomized (HYPOX) rats. GHRH (solid columns) or physiological saline (open columns) was injected 6 h after light onset. The duration of NREMS and REMS for 6‐h postinjection is depicted. Note that sleep is reduced in HYPOX rats (compare open columns between intact and HYPOX rats). Compared to baseline after physiological saline, however, GHRH continues to promote NREMS in the HYPOX rats but it fails to increase REMS.

Figure 3. Figure 3.

Schematic model showing possible interactions between the GHRH‐GH axis and the corticotropin‐releasing hormone (CRH) corticotropin axis in sleep modulation. CRH inhibits the somatotropic axis via somatostatin in the rat but the existence of a similar link is unclear in humans. The model also includes the cytokine, IL‐1. Low doses of IL‐1 enhance sleep in part via GHRH in the rat. High doses of IL1 cause sleep fragmentation and decreases in sleep in the rat; the well‐documented CRH‐releasing activity of IL‐1 might be involved in the sleep impairment. It is also not clear whether this model of IL‐1 action is specific to the species: for example a wide dose range of IL‐1 stimulates NREMS with little signs of sleep fragmentation in the rabbit. → indicates stimulation; ⊣ indicates inhibition.



Figure 1.

The diurnal rhythms of hypothalamic growth hormone‐releasing hormone (GHRH) content, GHRH mRNA expression, and the duration of nonrapid eye movement sleep (NREMS) in rats. Measurements obtained in groups of rats sacrificed or recorded in various time points are double‐plotted for two consecutive 24‐h days each consisting of a 12‐h light and a 12‐h dark period. Time 0 and Time 24 indicate the onset of the light periods. Dark periods are marked by horizontal black bars.



Figure 2.

Effects of systemic injection of GHRH (0.5 g/kg) on sleep in intact and hypophysectomized (HYPOX) rats. GHRH (solid columns) or physiological saline (open columns) was injected 6 h after light onset. The duration of NREMS and REMS for 6‐h postinjection is depicted. Note that sleep is reduced in HYPOX rats (compare open columns between intact and HYPOX rats). Compared to baseline after physiological saline, however, GHRH continues to promote NREMS in the HYPOX rats but it fails to increase REMS.



Figure 3.

Schematic model showing possible interactions between the GHRH‐GH axis and the corticotropin‐releasing hormone (CRH) corticotropin axis in sleep modulation. CRH inhibits the somatotropic axis via somatostatin in the rat but the existence of a similar link is unclear in humans. The model also includes the cytokine, IL‐1. Low doses of IL‐1 enhance sleep in part via GHRH in the rat. High doses of IL1 cause sleep fragmentation and decreases in sleep in the rat; the well‐documented CRH‐releasing activity of IL‐1 might be involved in the sleep impairment. It is also not clear whether this model of IL‐1 action is specific to the species: for example a wide dose range of IL‐1 stimulates NREMS with little signs of sleep fragmentation in the rabbit. → indicates stimulation; ⊣ indicates inhibition.

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Ferenc Obál, James M. Krueger. Hormones, Cytokines, and Sleep. Compr Physiol 2011, Supplement 23: Handbook of Physiology, The Endocrine System, Coping with the Environment: Neural and Endocrine Mechanisms: 331-349. First published in print 2001. doi: 10.1002/cphy.cp070416