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Performing your original search, crh memory, in PubMed will retrieve 54 records.
Neurobiol Learn Mem. 2008 May;89(4):370-8. Epub 2007 Dec 20.
Post-training administration of corticotropin-releasing hormone (CRH) enhances retention of a spatial memory through a noradrenergic mechanism in male rats.
Row BW, Dohanich GP.
Department of Pediatrics, Kosair Children's Hospital Research Institute, University of Louisville, Louisville, KY 40202, USA.
Hormones released in response to stress play important roles in cognition. In the present study, the effects of the stress peptide, corticotropin-releasing hormone (CRH), on spatial reference memory were assessed following post-training administration. Adult Long-Evans male rats were trained for 6 days on a standard water maze task of reference memory in which animals must learn and remember the fixed location of a hidden, submerged platform. Each day, immediately following three training trials, rats received bilateral infusions of CRH into the lateral ventricles over a range of doses (0.1, 0.33, 1.0, 3.3 microg) or a vehicle solution. Post-training infusions of CRH improved retention as indicated by significantly shorter latencies and path lengths to locate the hidden platform on the first training (retention) trial of days 2 and 3. Additionally, post-training administration of CRH increased spatial bias during probe trials as measured by proximity to the platform location. CRH did not enhance performance on retention or probe trials when administered 2h after daily training indicating that CRH facilitated consolidation specifically. The effects of CRH were attenuated by intraventricular co-administration of the beta-adrenergic antagonist, propanolol, at bilateral doses that had no effect on retention alone (0.1, 1.0 microg). Results indicate that post-training administration of CRH enhanced spatial memory as measured in a water maze, and this effect was mediated, at least partly, by a noradrenergic mechanism.
PMID: 18086539 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms, Substances
http://www.ncbi.nlm.nih.gov/pubmed/18086539
Norepinephrine
From Wikipedia, the free encyclopedia
Noradrenaline (BAN) (abbreviated NA or NAd) or norepinephrine (INN) (abbreviated norepi or NE) is a catecholamine with dual roles as a hormone and a neurotransmitter.[2]
As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle.
However, when norepinephrine acts as a drug it will increase blood pressure by its prominent increasing effects on the vascular tone from α-adrenergic receptor activation. The resulting increase in vascular resistance triggers a compensatory reflex that overcomes its direct stimulatory effects on the heart, called the baroreceptor reflex, which results in a drop in heart rate called reflex bradycardia.
Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase.[3] It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system where it is released from noradrenergic neurons. The actions of norepinephrine are carried out via the binding to adrenergic receptors.
SEE MORE! at:
http://en.wikipedia.org/wiki/Norepinephrine
SEE ALSO:
Dopamine
http://en.wikipedia.org/wiki/Dopamine
Prolactin
http://en.wikipedia.org/wiki/Prolactin
Copyright © 1999 Elsevier Science Inc. All rights reserved.
Original Articles
Changes in hippocampal theta following intrahippocampal corticotropin-releasing hormone (CRH) infusions in the rat
Rudie Kortekaas, , a, Brenda Costalla and James W. Smythea
a Department of Pharmacology, University of Bradford, Bradford, UK
Received 7 October 1998;
revised 2 February 1999;
accepted 2 February 1999.
Available online 1 June 1999.
Abstract
Hippocampal theta activity is a large amplitude, sinusoidal wave that occurs during attentive immobility and exploratory behaviour in the rat, and it is thought to be involved in memory formation.
Recent reports suggest that corticotropin-releasing hormone (CRH) has pro-mnemonic effects in rodents.
(A mnemonic device (pronounced /nɨˈmɒnɨk/[1]) is a mind memory and/or learning aid. Commonly, mnemonics are verbal—such as a very short poem or a special word used to help a person remember something - wikipedia)
Because memory-enhancing substances/manipulations generally alter either theta frequencies or amplitudes, these variables were monitored in urethane-anaesthetised rats following intra-hippocampal infusions of CRH.
Adult male, Lister hooded rats were implanted with a hippocampal recording electrode and a guide cannula, both aimed at the dentate gyrus.
When CRH was infused into the hippocampus, the main change in the hippocampal EEG was a slow onset increase in the amplitude of spontaneous theta and, paradoxically, a significant decrease in the amount of time spent displaying theta.
These data suggest that CRH has the ability to modulate ongoing hippocampal theta, but, considering the slow effect, the involvement of hippocampal CRH receptors is suspect. Regardless of locus, the described electrophysiological changes suggest that hippocampal cholinergic systems may play a role in the memory-enhancing effects of CRH.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYT-3WKY1S9-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1066745569&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=ed79d8585decfce3507a3675c4a5f584
Tuesday, October 27, 2009
Involvement of the corticotropin-releasing hormone system in the pathogenesis of acne vulgaris
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Involvement of the corticotropin-releasing hormone system in the pathogenesis of acne vulgaris.
Centre of Dermatovenereology, Vilnius University Hospital, Santariskiu Klinikos, Vilnius, Lithuania.
Comment in:
Br J Dermatol. 2009 Feb;160(2):229-32.
BACKGROUND:
The sebaceous gland exhibits an independent peripheral endocrine function and expresses receptors for neuropeptides.
Previous reports have confirmed the presence of a complete corticotropin-releasing hormone (CRH) system in human sebocytes in vitro.
The capability of hypothalamic CRH to induce lipid synthesis, induce steroidogenesis and interact with testosterone and growth hormone implicates a possibility of its involvement in the clinical development of acne.
OBJECTIVES:
The purpose of the study was to detect expression changes of CRH/CRH binding protein (CRHBP)/CRH receptors (CRHRs) in acne-involved skin, especially in the sebaceous glands.
METHODS:
Expression of CRH/CRHBP/CRHRs was analysed by immunohistochemistry in biopsies from facial skin of 33 patients with acne, noninvolved thigh skin of the same patients and normal skin of eight age-matched healthy volunteers.
RESULTS:
Very strong positive reaction for CRH was observed in acne-involved skin in all types of sebaceous gland cells, irrespective of their differentiation stage, whereas in noninvolved and normal skin sebaceous glands exhibited a weaker CRH staining depending upon the differentiation stage of sebocytes.
The strongest reaction for CRHBP (binding protein) in acne-involved sebaceous glands was in differentiating sebocytes.
CRHR-1 and CRHR-2 exhibited the strongest expression in sweat glands and sebaceous glands, respectively.
CONCLUSIONS:
Expression of the complete CRH system is abundant in acne-involved skin, especially in the sebaceous glands, possibly activating pathways which affect immune and inflammatory processes leading to the development and stress-induced exacerbation of acne.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=19077080%5Buid%5D
Differential Expression of a Cutaneous Corticotropin-
Releasing Hormone System
Neuroimmunoendocrine circuitry of the ‘brain-skin connection’
aDepartment of Dermatology, University Hospital Schleswig-Holstein, Campus Lübeck, University of Lübeck, D-23538 Lübeck, Germany
bDepartments of Pharmacology & Experimental Therapeutics, Biochemistry and Internal Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
cBiomedical Research Center, Charité – University Medicine Berlin, D-13353 Berlin, Germany
Available online 2 November 2005.
The skin offers an ideally suited, clinically relevant model for studying the crossroads between peripheral and systemic responses to stress.
Involvement of the corticotropin-releasing hormone system in the pathogenesis of acne vulgaris.
Br J Dermatol. 2009 Feb;160(2):345-52. Epub 2008 Dec 10.
Ganceviciene R, Graziene V, Fimmel S, Zouboulis CC.
Ganceviciene R, Graziene V, Fimmel S, Zouboulis CC.
Centre of Dermatovenereology, Vilnius University Hospital, Santariskiu Klinikos, Vilnius, Lithuania.
Comment in:
Br J Dermatol. 2009 Feb;160(2):229-32.
BACKGROUND:
The sebaceous gland exhibits an independent peripheral endocrine function and expresses receptors for neuropeptides.
Previous reports have confirmed the presence of a complete corticotropin-releasing hormone (CRH) system in human sebocytes in vitro.
The capability of hypothalamic CRH to induce lipid synthesis, induce steroidogenesis and interact with testosterone and growth hormone implicates a possibility of its involvement in the clinical development of acne.
OBJECTIVES:
The purpose of the study was to detect expression changes of CRH/CRH binding protein (CRHBP)/CRH receptors (CRHRs) in acne-involved skin, especially in the sebaceous glands.
METHODS:
Expression of CRH/CRHBP/CRHRs was analysed by immunohistochemistry in biopsies from facial skin of 33 patients with acne, noninvolved thigh skin of the same patients and normal skin of eight age-matched healthy volunteers.
RESULTS:
Very strong positive reaction for CRH was observed in acne-involved skin in all types of sebaceous gland cells, irrespective of their differentiation stage, whereas in noninvolved and normal skin sebaceous glands exhibited a weaker CRH staining depending upon the differentiation stage of sebocytes.
The strongest reaction for CRHBP (binding protein) in acne-involved sebaceous glands was in differentiating sebocytes.
CRHR-1 and CRHR-2 exhibited the strongest expression in sweat glands and sebaceous glands, respectively.
CONCLUSIONS:
Expression of the complete CRH system is abundant in acne-involved skin, especially in the sebaceous glands, possibly activating pathways which affect immune and inflammatory processes leading to the development and stress-induced exacerbation of acne.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=19077080%5Buid%5D
SEE ALSO (pdf file):
Differential Expression of a Cutaneous Corticotropin-
Releasing Hormone System
Copyright © 2005 Elsevier Ltd All rights reserved.
Neuroimmunoendocrine circuitry of the ‘brain-skin connection’
aDepartment of Dermatology, University Hospital Schleswig-Holstein, Campus Lübeck, University of Lübeck, D-23538 Lübeck, Germany
bDepartments of Pharmacology & Experimental Therapeutics, Biochemistry and Internal Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
cBiomedical Research Center, Charité – University Medicine Berlin, D-13353 Berlin, Germany
Available online 2 November 2005.
The skin offers an ideally suited, clinically relevant model for studying the crossroads between peripheral and systemic responses to stress.
A ‘brain–skin connection’ with local neuroimmunoendocrine circuitry underlies the pathogenesis of allergic and inflammatory skin diseases, triggered or aggravated by stress.
In stressed mice, corticotropin-releasing hormone (CRH), nerve growth factor, neurotensin, substance P and mast cells are recruited hierarchically to induce neurogenic skin inflammation, which inhibits hair growth.
The hair follicle is both a target and a source for immunomodulatory stress mediators, and has an equivalent of the hypothalamus–pituitary–adrenal axis.
Thus, the skin and its appendages enable the study of complex neuroimmunoendocrine responses that peripheral tissues launch upon stress exposure, as a basis for identifying new targets for therapeutic stress intervention.
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