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Increased susceptibility to disseminated Candidiasis in interleukin-6 deficient mice.
van Enckevoort F, Netea MG, Hermus A, Sweep CG, van der Meer JW, Kullberg BJ; Interscience Conference on Antimicrobial Agents and Chemotherapy. Abstr Intersci Conf Antimicrob Agents Chemother Intersci Conf Antimicrob Agents Chemother. 1998 Sep 24-27; 38: 296 (abstract no. G-43).
Univ. Hosp. Nijmegen, The Netherlands.
Interleukin-6 (IL-6) is a multifunctional cytokine that regulates multiple aspects of the innate immune response. It has been recently shown that endogenous IL-6 is crucial for an efficient defense against severe infections with Gram- negative and Gram-positive bacteria. The aim of the present study was to investigate the role of endogenous IL-6 in the defense against infection with the yeast Candida albicans. When infected with 3x10(5) CFU/mouse, IL-6 deficient mice (IL-6-/-) had a significantly decreased survival when compared with IL-6+/+ controls (30 vs. 70%, p<0.05). href="http://gateway.nlm.nih.gov/MeetingAbstracts/102188063.html">http://gateway.nlm.nih.gov/MeetingAbstracts/102188063.html
Peripheral corticotropin-releasing factor mediates the elevation of plasma IL-6 by immobilization stress in rats
Auteur(s) / Author(s)ANDO T. (1) ; RIVIER J. (2) ; YANAIHARA H. (1) ; ARIMURA A. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)(1) United States-Japan Biomedical Research Laboratories, Tulane University Hebert Center, Belle Chasse, Louisiana 70037-3001, ETATS-UNIS(2) Peptide Biology Laboratory, Salk Institute, La Jolla, California 92037, ETATS-UNIS
Résumé / AbstractWe previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [D-Phe12,Nle21,38,CαMeLeu37]-anti-human rat (h/r) CRF12-41 (1.5 mg/kg) or cyclo(30-33)[D-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12-41 (Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 μg/kg) or rat urocortin (10 and 100 μg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 μg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.
http://cat.inist.fr/?aModele=afficheN&cpsidt=1770729
Friday, October 16, 2009
Protective effect of alprazolam against sleep deprivation-induced behavior alterations and oxidative damage in mice
Protective effect of alprazolam against sleep deprivation-induced behavior alterations and oxidative damage in mice.
Singh A, Kumar A.
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.
Sleep deprivation is considered as a risk factor for various diseases.
Sleep deprivation leads to behavioral, hormonal, neurochemical and biochemical alterations in the animals.
The present study was designed to explore the possible involvement of GABAergic mechanism in protective effect of alprazolam against 72h sleep deprivation-induced behavior alterations and oxidative damage in mice.
In the present study, sleep deprivation caused
anxiety-like behavior,
weight loss,
impaired ambulatory movements and
oxidative damage
as indicated by
increase in lipid peroxidation,
nitrite level and
depletion of reduced glutathione and catalase activity
in sleep-deprived mice brain.
Treatment with alprazolam (0.25 and 0.5 mg/kg, ip) significantly improved behavioral alterations.
Biochemically, alprazolam treatment significantly restored depleted reduced glutathione, catalase activity,
reversed raised lipid peroxidation and nitrite level.
Combination of flumazenil (0.5 mg/kg) and picrotoxin (0.5 mg/kg) with lower dose of alprazolam (0.25mg/kg) significantly antagonized protective effect of alprazolam.
However, combination of muscimol (0.05 mg/kg) with alprazolam (0.25 mg/kg, ip) potentiated protective effect of alprazolam.
On the basis of these results, it might be suggested that alprazolam might produce protective effect by involving GABAergic system against sleep deprivation-induced behavior alterations and related oxidative damage.
PMID: 18280601 [PubMed - indexed for MEDLINE]
Glutathione
From Wikipedia, the free encyclopedia
Glutathione (GSH) is a tripeptide. It contains an unusual peptide linkage between the amine group of cysteine and the carboxyl group of the glutamate side chain. Glutathione, an antioxidant, helps protect cells from reactive oxygen species such as free radicals and peroxides.[2] Glutathione is also nucleophile at sulfur and attacks poisonous conjugate acceptors.
Thiol groups are kept in a reduced state at a concentration of approximately ~5 mM in animal cells. In effect, glutathione reduces any disulfide bond formed within cytoplasmic proteins to cysteines by acting as an electron donor. In the process, glutathione is converted to its oxidized form glutathione disulfide (GSSG). Glutathione is found almost exclusively in its reduced form, since the enzyme that reverts it from its oxidized form, glutathione reductase, is constitutively active and inducible upon oxidative stress. In fact, the ratio of reduced glutathione to oxidized glutathione within cells is often used scientifically as a measure of cellular toxicity.[3]
Function in animals
GSH is known as a substrate in both conjugation reactions and reduction reactions, catalyzed by glutathione S-transferase enzymes in cytosol, microsomes, and mitochondria. However, it is also capable of participating in non-enzymatic conjugation with some chemicals, as in the case of N-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450-reactive metabolite formed by paracetamol (or acetaminophen as it is known in the US), that becomes toxic when GSH is depleted by an overdose of acetaminophen.
Glutathione conjugates to NAPQI and helps to detoxify it, in this capacity protects cellular protein thiol groups, which would otherwise become covalently modified; when all GSH has been spent, NAPQI begins to react with the cellular proteins, killing the cells in the process.
The preferred treatment for an overdose of this painkiller is the administration (usually in atomized form) of N-acetyl-L-cysteine, which is processed by cells to L-cysteine and used in the de novo synthesis of GSH.
Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase.
It is also important as a hydrophilic molecule that is added to lipophilic toxins and waste in the liver during biotransformation before they can become part of the bile. Glutathione is also needed for the detoxification of methylglyoxal, a toxin produced as a by-product of metabolism.
This detoxification reaction is carried out by the glyoxalase system. Glyoxalase I (EC 4.4.1.5) catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-lactoyl-glutathione. Glyoxalase II (EC 3.1.2.6) catalyzes the hydrolysis of S-D-lactoyl-glutathione to glutathione and D-lactic acid.
Glutathione has recently been used as an inhibitor of melanin in the cosmetics industry. In countries like the Philippines, this product is sold as a whitening soap. Glutathione competitively inhibits melanin synthesis in the reaction of tyrosinase and L-DOPA by interrupting L-DOPA's ability to bind to tyrosinase during melanin synthesis.
The inhibition of melanin synthesis was reversed by increasing the concentration of L-DOPA, but not by increasing tyrosinase. Although the synthesized melanin was aggregated within 1 h, the aggregation was inhibited by the addition of glutathione.
These results indicate that glutathione inhibits the synthesis and agglutination of melanin by interrupting the function of L-DOPA. "[17]
silymarin or milk thistle has also demonstrated an ability to replenish glutathione levels!!!
Glutathione is a tightly regulated intracellular constituent and is limited in its production by negative feedback inhibition of its own synthesis through the enzyme gamma-glutamylcysteine synthetase, thus greatly minimizing any possibility of overdosage.
Glutathione augmentation is a strategy developed to address states of glutathione deficiency, high oxidative stress, immune deficiency, and xenobiotic overload in which glutathione plays a part in the detoxification of the xenobiotic in question.
Glutathione deficiency states include, but are not limited to: HIV/AIDS, chemical and infectious hepatitis, prostate and other cancers, cataracts, Alzheimer's, Parkinsons, chronic obstructive pulmonary disease, asthma, radiation poisoning, malnutritive states, arduous physical stress, aging, and has been associated with sub-optimal immune response. Many clinical pathologies are associated with oxidative stress and are elaborated upon in numerous medical references.[44]
Low glutathione is also strongly implicated in wasting and negative nitrogen balance, [45] notably as seen in cancer, AIDS, sepsis, trauma, burns and even athletic overtraining. Glutathione supplementation can oppose this process and in AIDS, for example, result in improved survival rates.[46]
http://en.wikipedia.org/wiki/Glutathione
the 'organ Km' for glutathione in the liver is approximately 0.5 mumol/g of liver, so that the hepatic glutathione conjugation rate is decreased only at severe glutathione depletion.
Singh A, Kumar A.
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.
Sleep deprivation is considered as a risk factor for various diseases.
Sleep deprivation leads to behavioral, hormonal, neurochemical and biochemical alterations in the animals.
The present study was designed to explore the possible involvement of GABAergic mechanism in protective effect of alprazolam against 72h sleep deprivation-induced behavior alterations and oxidative damage in mice.
In the present study, sleep deprivation caused
anxiety-like behavior,
weight loss,
impaired ambulatory movements and
oxidative damage
as indicated by
increase in lipid peroxidation,
nitrite level and
depletion of reduced glutathione and catalase activity
in sleep-deprived mice brain.
Treatment with alprazolam (0.25 and 0.5 mg/kg, ip) significantly improved behavioral alterations.
Biochemically, alprazolam treatment significantly restored depleted reduced glutathione, catalase activity,
reversed raised lipid peroxidation and nitrite level.
Combination of flumazenil (0.5 mg/kg) and picrotoxin (0.5 mg/kg) with lower dose of alprazolam (0.25mg/kg) significantly antagonized protective effect of alprazolam.
However, combination of muscimol (0.05 mg/kg) with alprazolam (0.25 mg/kg, ip) potentiated protective effect of alprazolam.
On the basis of these results, it might be suggested that alprazolam might produce protective effect by involving GABAergic system against sleep deprivation-induced behavior alterations and related oxidative damage.
PMID: 18280601 [PubMed - indexed for MEDLINE]
Glutathione
From Wikipedia, the free encyclopedia
Glutathione (GSH) is a tripeptide. It contains an unusual peptide linkage between the amine group of cysteine and the carboxyl group of the glutamate side chain. Glutathione, an antioxidant, helps protect cells from reactive oxygen species such as free radicals and peroxides.[2] Glutathione is also nucleophile at sulfur and attacks poisonous conjugate acceptors.
Thiol groups are kept in a reduced state at a concentration of approximately ~5 mM in animal cells. In effect, glutathione reduces any disulfide bond formed within cytoplasmic proteins to cysteines by acting as an electron donor. In the process, glutathione is converted to its oxidized form glutathione disulfide (GSSG). Glutathione is found almost exclusively in its reduced form, since the enzyme that reverts it from its oxidized form, glutathione reductase, is constitutively active and inducible upon oxidative stress. In fact, the ratio of reduced glutathione to oxidized glutathione within cells is often used scientifically as a measure of cellular toxicity.[3]
Function in animals
GSH is known as a substrate in both conjugation reactions and reduction reactions, catalyzed by glutathione S-transferase enzymes in cytosol, microsomes, and mitochondria. However, it is also capable of participating in non-enzymatic conjugation with some chemicals, as in the case of N-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450-reactive metabolite formed by paracetamol (or acetaminophen as it is known in the US), that becomes toxic when GSH is depleted by an overdose of acetaminophen.
Glutathione conjugates to NAPQI and helps to detoxify it, in this capacity protects cellular protein thiol groups, which would otherwise become covalently modified; when all GSH has been spent, NAPQI begins to react with the cellular proteins, killing the cells in the process.
The preferred treatment for an overdose of this painkiller is the administration (usually in atomized form) of N-acetyl-L-cysteine, which is processed by cells to L-cysteine and used in the de novo synthesis of GSH.
Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase.
It is also important as a hydrophilic molecule that is added to lipophilic toxins and waste in the liver during biotransformation before they can become part of the bile. Glutathione is also needed for the detoxification of methylglyoxal, a toxin produced as a by-product of metabolism.
This detoxification reaction is carried out by the glyoxalase system. Glyoxalase I (EC 4.4.1.5) catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-lactoyl-glutathione. Glyoxalase II (EC 3.1.2.6) catalyzes the hydrolysis of S-D-lactoyl-glutathione to glutathione and D-lactic acid.
Glutathione has recently been used as an inhibitor of melanin in the cosmetics industry. In countries like the Philippines, this product is sold as a whitening soap. Glutathione competitively inhibits melanin synthesis in the reaction of tyrosinase and L-DOPA by interrupting L-DOPA's ability to bind to tyrosinase during melanin synthesis.
The inhibition of melanin synthesis was reversed by increasing the concentration of L-DOPA, but not by increasing tyrosinase. Although the synthesized melanin was aggregated within 1 h, the aggregation was inhibited by the addition of glutathione.
These results indicate that glutathione inhibits the synthesis and agglutination of melanin by interrupting the function of L-DOPA. "[17]
silymarin or milk thistle has also demonstrated an ability to replenish glutathione levels!!!
Glutathione is a tightly regulated intracellular constituent and is limited in its production by negative feedback inhibition of its own synthesis through the enzyme gamma-glutamylcysteine synthetase, thus greatly minimizing any possibility of overdosage.
Glutathione augmentation is a strategy developed to address states of glutathione deficiency, high oxidative stress, immune deficiency, and xenobiotic overload in which glutathione plays a part in the detoxification of the xenobiotic in question.
Glutathione deficiency states include, but are not limited to: HIV/AIDS, chemical and infectious hepatitis, prostate and other cancers, cataracts, Alzheimer's, Parkinsons, chronic obstructive pulmonary disease, asthma, radiation poisoning, malnutritive states, arduous physical stress, aging, and has been associated with sub-optimal immune response. Many clinical pathologies are associated with oxidative stress and are elaborated upon in numerous medical references.[44]
Low glutathione is also strongly implicated in wasting and negative nitrogen balance, [45] notably as seen in cancer, AIDS, sepsis, trauma, burns and even athletic overtraining. Glutathione supplementation can oppose this process and in AIDS, for example, result in improved survival rates.[46]
http://en.wikipedia.org/wiki/Glutathione
the 'organ Km' for glutathione in the liver is approximately 0.5 mumol/g of liver, so that the hepatic glutathione conjugation rate is decreased only at severe glutathione depletion.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1132802/
Catalase
From Wikipedia, the free encyclopedia
Catalase is a common enzyme found in nearly all living organisms which are exposed to oxygen, where it functions to catalyze the decomposition of hydrogen peroxide to water and oxygen.[1]
Grey hair
According to recent scientific studies, low levels of catalase may play a role in the greying process of human hair. Hydrogen peroxide is naturally produced by the body and catalase breaks it down. If there is a dip in catalase levels, hydrogen peroxide cannot be broken down. This causes the hydrogen peroxide to bleach the hair from the inside out. Scientists believe this finding may someday lead to "anti" greying treatments for aging hair.[30][31][32]
http://en.wikipedia.org/wiki/Catalase
STRESS-INDUCED SLEEP DEPRIVATION MODIFIES CORTICOTROPIN RELEASING FACTOR (CRF) LEVELS
Copyright © 1997 The Italian Pharmacological Society. Published by Elsevier Science Ltd.
Regular Article
STRESS-INDUCED SLEEP DEPRIVATION MODIFIES CORTICOTROPIN RELEASING FACTOR (CRF) LEVELS AND CRF BINDING IN RAT BRAIN AND PITUITARY*1
PAOLA FADDAa, f1 and WALTER FRATTAb
a ‘B.B. Brodie’ Department of Neuroscience, University of Cagliari, Cagliari, Italy
b Center for Neuropharmacology, National Research Council University of Cagliari, Cagliari, Italy
Accepted 2 April 1997. ;
Available online 15 April 2002.
Abstract
Electroencephalographic (EEG) studies have shown that corticotropin-releasing factor (CRF) administration induces EEG activation, decreases sleep time both in rats and humans and modifies the sleep pattern in sleep deprived rats.
In the present study we have investigated whether CRF neuronal activity could be altered in a situation of disrupted sleep-wake cycle.
Sleep deprivation (SD) was induced by keeping the rat for 72 h on a small platform (7 cm) surrounded by water.
Immediately after the SD period rats were killed and CRF levels and CRF receptor binding were evaluated in different brain areas.
A marked increase in CRF levels was present in the striatum (+224%), limbic areas (+144%) and pituitary (+42%) whereas the hypothalamic CRF content was reduced (−57%).
A significant decrease in CRF binding was found in the striatum (−33%) and pituitary (−38%) of sleep deprived rats.
These results indicate that CRF neuronal activity is stimulated by SD, suggesting that CRF might play an important role in the physiological regulation of the sleep-wake cycle and that an altered CRF neuronal activity might be involved in behavioral modifications related to sleep disturbances.
Author Keywords: Sleep deprivation; corticotropin-releasing factor; limbic system; striatum; rat
*1 De Souza, EBNemeroff, CB
f1 Correspondence to: Paola Fadda, ‘B.B. Brodie’ Department of Neuroscience, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WP9-45KKVFG-2V&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1051469287&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=643478cc8d82373b16a116de18bfa062
Regular Article
STRESS-INDUCED SLEEP DEPRIVATION MODIFIES CORTICOTROPIN RELEASING FACTOR (CRF) LEVELS AND CRF BINDING IN RAT BRAIN AND PITUITARY*1
PAOLA FADDAa, f1 and WALTER FRATTAb
a ‘B.B. Brodie’ Department of Neuroscience, University of Cagliari, Cagliari, Italy
b Center for Neuropharmacology, National Research Council University of Cagliari, Cagliari, Italy
Accepted 2 April 1997. ;
Available online 15 April 2002.
Abstract
Electroencephalographic (EEG) studies have shown that corticotropin-releasing factor (CRF) administration induces EEG activation, decreases sleep time both in rats and humans and modifies the sleep pattern in sleep deprived rats.
In the present study we have investigated whether CRF neuronal activity could be altered in a situation of disrupted sleep-wake cycle.
Sleep deprivation (SD) was induced by keeping the rat for 72 h on a small platform (7 cm) surrounded by water.
Immediately after the SD period rats were killed and CRF levels and CRF receptor binding were evaluated in different brain areas.
A marked increase in CRF levels was present in the striatum (+224%), limbic areas (+144%) and pituitary (+42%) whereas the hypothalamic CRF content was reduced (−57%).
A significant decrease in CRF binding was found in the striatum (−33%) and pituitary (−38%) of sleep deprived rats.
These results indicate that CRF neuronal activity is stimulated by SD, suggesting that CRF might play an important role in the physiological regulation of the sleep-wake cycle and that an altered CRF neuronal activity might be involved in behavioral modifications related to sleep disturbances.
Author Keywords: Sleep deprivation; corticotropin-releasing factor; limbic system; striatum; rat
*1 De Souza, EBNemeroff, CB
f1 Correspondence to: Paola Fadda, ‘B.B. Brodie’ Department of Neuroscience, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WP9-45KKVFG-2V&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1051469287&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=643478cc8d82373b16a116de18bfa062
Immobilisation stress induces a paradoxical sleep rebound in rat
Immobilisation stress induces a paradoxical sleep rebound in rat
Rampin C, Cespuglio R, Chastrette N, Jouvet M.
Département de Médecine Expérimentale, INSERM U 52, CNRS URA 1195, Université Claude Bernard, Lyons, France.
An immobilisation stress (IS) of 2 h applied to rats at the beginning of the dark period (12 h), i.e. when the animals are more active, induces during the 10 consecutive h a significant rebound (+92%) of paradoxical sleep (PS) while slow-wave sleep state (SWS) is poorly affected. Two h of sleep deprivation, also applied at the beginning of the dark period and realized either by the platform technique or by maintaining the animals awake with gentle handling, do not affect significantly subsequent SWS and PS. Finally, when repetitive IS are inflicted to the animals (one IS of 2 h every 3 days) an attenuation of the PS rebound is observed.
These data suggest that a qualitative aspect of the waking state as in an intense stressful situation might be the source of a hormonal process inducing a PS (paradoxical sleep) excess.
PMID: 1922920 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/1922920
Involvement of stress in the sleep rebound mechanism induced by sleep deprivation in the rat: use of alpha-helical CRH(9-41)
González, M M del C.; Valatx, J-L
Abstract
A previous study demonstrated the efficacy of the corticotropin-releasing hormone (CRH) receptor antagonist, [alpha] -helical CRH (9-41), in blocking the paradoxical sleep increase induced by stress.
In the present study, this peptide was used to evaluate the involvement of the stress component of the sleep deprivation, in the paradoxical sleep rebound.
Rats were subjected for 10 h to the classical water-tank sleep-deprivation technique and were given, every 2 h throughout the sleep deprivation period, intracerebroventricular injections of either 100 [micro]g/5 [micro]I of a-helical CRH (9-41) or vehicle alone.
Continuous recordings showed that antagonist treatment decreased the PS rebound, but not the SWS rebound, following sleep deprivation.
These findings suggest that, in the water-tank sleep deprivation method, stress, acting via CRH activation, is the main factor inducing the paradoxical sleep rebound.
(C) 1998 Lippincott Williams & Wilkins, Inc.
http://journals.lww.com/behaviouralpharm/Abstract/1998/12000/Involvement_of_stress_in_the_sleep_rebound.1.aspx
Rampin C, Cespuglio R, Chastrette N, Jouvet M.
Département de Médecine Expérimentale, INSERM U 52, CNRS URA 1195, Université Claude Bernard, Lyons, France.
An immobilisation stress (IS) of 2 h applied to rats at the beginning of the dark period (12 h), i.e. when the animals are more active, induces during the 10 consecutive h a significant rebound (+92%) of paradoxical sleep (PS) while slow-wave sleep state (SWS) is poorly affected. Two h of sleep deprivation, also applied at the beginning of the dark period and realized either by the platform technique or by maintaining the animals awake with gentle handling, do not affect significantly subsequent SWS and PS. Finally, when repetitive IS are inflicted to the animals (one IS of 2 h every 3 days) an attenuation of the PS rebound is observed.
These data suggest that a qualitative aspect of the waking state as in an intense stressful situation might be the source of a hormonal process inducing a PS (paradoxical sleep) excess.
PMID: 1922920 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/1922920
Involvement of stress in the sleep rebound mechanism induced by sleep deprivation in the rat: use of alpha-helical CRH(9-41)
González, M M del C.; Valatx, J-L
Abstract
A previous study demonstrated the efficacy of the corticotropin-releasing hormone (CRH) receptor antagonist, [alpha] -helical CRH (9-41), in blocking the paradoxical sleep increase induced by stress.
In the present study, this peptide was used to evaluate the involvement of the stress component of the sleep deprivation, in the paradoxical sleep rebound.
Rats were subjected for 10 h to the classical water-tank sleep-deprivation technique and were given, every 2 h throughout the sleep deprivation period, intracerebroventricular injections of either 100 [micro]g/5 [micro]I of a-helical CRH (9-41) or vehicle alone.
Continuous recordings showed that antagonist treatment decreased the PS rebound, but not the SWS rebound, following sleep deprivation.
These findings suggest that, in the water-tank sleep deprivation method, stress, acting via CRH activation, is the main factor inducing the paradoxical sleep rebound.
(C) 1998 Lippincott Williams & Wilkins, Inc.
http://journals.lww.com/behaviouralpharm/Abstract/1998/12000/Involvement_of_stress_in_the_sleep_rebound.1.aspx
Sleep deprivation effects on the activity of the hypothalamic–pituitary–adrenal and growth axes: potential clinical implications
Sleep deprivation effects on the activity of the hypothalamic–pituitary–adrenal and growth axes: potential clinical implications
Alexandros N. Vgontzas , George Mastorakos , Edward O. Bixler , Anthony Kales , Philip W. Gold & George P. Chrousos
1 Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University, Hershey, USA, 2 Endocrine Unit, Evgenidion Hospital, Athens University, Athens, Greece, 3 Clinical Neuroendocrinology Branch, National Institute of Mental Health, Bethesda, USA, 4 Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, USA
Correspondence to: Dr Alexandros N. Vgontzas Sleep Research and Treatment Center, Department of Psychiatry Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, PA 17033, USA. Fax: +1 (717) 531 6491.
Copyright 1999 Blackwell Science Ltd
ABSTRACT
OBJECTIVES
Although several studies have shown that sleep deprivation is associated with increased slow wave sleep during the recovery night, the effects of sleep deprivation on cortisol and growth hormone (GH) secretion the next day and recovery night have not been assessed systematically. We hypothesized that increased slow wave sleep postsleep deprivation is associated with decreased cortisol levels and that the enhanced GH secretion is driven by the decreased activity of the HPA axis.
DESIGN AND SUBJECTS
After four consecutive nights in the Sleep Laboratory, 10 healthy young men were totally deprived of sleep during the fifth night, and then allowed to sleep again on nights six and seven. Twenty-four hour blood sampling was performed serially every 30 minutes on the fourth day, immediately following the previous night of sleep and on the sixth day, immediately after sleep deprivation.
MEASUREMENT
Eight-hour sleep laboratory recording, including electroencephologram, electro-oculogram and electromyogram. Plasma cortisol and GH levels using specific immunoassay techniques.
RESULTS
Mean plasma and time-integrated (AUC) cortisol levels were lower during the postdeprivation nighttime period than on the fourth night (P < class="invisible-anchor" name="h005">
CONCLUSION
We conclude that sleep deprivation results in a significant reduction of cortisol secretion the next day and this reduction appears to be, to a large extent, driven by the increase of slow wave sleep during the recovery night.
We propose that reduction of CRH and cortisol secretion may be the mechanism through which sleep deprivation relieves depression temporarily.
Furthermore, deep sleep has an inhibitory effect on the HPA axis while it enhances the activity of the GH axis. In contrast, sleep disturbance has a stimulatory effect on the HPA axis and a suppressive effect on the GH axis.
These results are consistent with the observed hypocortisolism in idiopathic hypersomnia and HPA axis relative activation in chronic insomnia.
Finally, our findings support previous hypotheses about the restitution and immunoenhancement role of slow wave (deep) sleep.
Alexandros N. Vgontzas , George Mastorakos , Edward O. Bixler , Anthony Kales , Philip W. Gold & George P. Chrousos
1 Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University, Hershey, USA, 2 Endocrine Unit, Evgenidion Hospital, Athens University, Athens, Greece, 3 Clinical Neuroendocrinology Branch, National Institute of Mental Health, Bethesda, USA, 4 Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, USA
Correspondence to: Dr Alexandros N. Vgontzas Sleep Research and Treatment Center, Department of Psychiatry Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, PA 17033, USA. Fax: +1 (717) 531 6491.
Copyright 1999 Blackwell Science Ltd
ABSTRACT
OBJECTIVES
Although several studies have shown that sleep deprivation is associated with increased slow wave sleep during the recovery night, the effects of sleep deprivation on cortisol and growth hormone (GH) secretion the next day and recovery night have not been assessed systematically. We hypothesized that increased slow wave sleep postsleep deprivation is associated with decreased cortisol levels and that the enhanced GH secretion is driven by the decreased activity of the HPA axis.
DESIGN AND SUBJECTS
After four consecutive nights in the Sleep Laboratory, 10 healthy young men were totally deprived of sleep during the fifth night, and then allowed to sleep again on nights six and seven. Twenty-four hour blood sampling was performed serially every 30 minutes on the fourth day, immediately following the previous night of sleep and on the sixth day, immediately after sleep deprivation.
MEASUREMENT
Eight-hour sleep laboratory recording, including electroencephologram, electro-oculogram and electromyogram. Plasma cortisol and GH levels using specific immunoassay techniques.
RESULTS
Mean plasma and time-integrated (AUC) cortisol levels were lower during the postdeprivation nighttime period than on the fourth night (P < class="invisible-anchor" name="h005">
CONCLUSION
We conclude that sleep deprivation results in a significant reduction of cortisol secretion the next day and this reduction appears to be, to a large extent, driven by the increase of slow wave sleep during the recovery night.
We propose that reduction of CRH and cortisol secretion may be the mechanism through which sleep deprivation relieves depression temporarily.
Furthermore, deep sleep has an inhibitory effect on the HPA axis while it enhances the activity of the GH axis. In contrast, sleep disturbance has a stimulatory effect on the HPA axis and a suppressive effect on the GH axis.
These results are consistent with the observed hypocortisolism in idiopathic hypersomnia and HPA axis relative activation in chronic insomnia.
Finally, our findings support previous hypotheses about the restitution and immunoenhancement role of slow wave (deep) sleep.
http://www3.interscience.wiley.com/journal/118881160/abstract?CRETRY=1&SRETRY=0
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