Central administration of corticotropin-releasing factor induces tissue specific oxidative damage in chicks

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Central administration of corticotropin-releasing factor induces tissue specific oxidative damage in chicks
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  Central administration of corticotropin-releasing factor induces tissue speci fi coxidative damage in chicks Ahmad Mujahid ⁎ , Mitsuhiro Furuse Laboratory of Advanced Animal and Marine Bioresources, Faculty of Agriculture, Kyushu University, 6-10-1, Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan a b s t r a c ta r t i c l e i n f o  Article history: Received 20 July 2008Received in revised form 12 August 2008Accepted 13 August 2008Available online 22 August 2008 Keywords: CRFIntracerebroventricularOxidative damageMDANeonatal chick Corticotropin-releasing factor (CRF) modulates the activity of the hypothalamic – pituitary – adrenal (HPA) axis,and has a key role in mediating neuroendocrine effects which occur in response to stressful stimuli. We haverecentlyshown that intracerebroventricular (ICV) injection of CRF in neonatal chicks increased homeothermythat was associated with enhanced gene transcripts of mitochondrial fatty acid (FA) transport and oxidationenzymes in a tissue speci fi c manner. These observations prompted an investigation into the potential role of CRF in a state of oxidative damage in different tissues. We therefore, investigated whether CRF-inducedchanges in metabolism are accompanied by oxidative damage in the plasma, brain and other tissues.Neonatal chicks ( Gallus gallus ) with or without ICV-CRF (42 pmol) were kept at thermoneutral temperature(30 °C). After 3 h, malondialdehyde (MDA) was measured in the plasma, brain, heart, liver and skeletalmuscle (gastrocnemius). ICV-CRF signi fi cantly decreased the weight gain and feed consumption of chicks.Plasma, heart and liver revealed signi fi cantly higher MDA levels in chicks with ICV-CRF as compared to thatof control chicks, but this pattern was not observed in the brain and muscle. Gene transcripts of enzymesinvolved in mitochondrial FA transport and oxidation, and 3-hydroxyacyl CoA dehydrogenase and citratesynthase enzyme activities in the brainwere not changed by ICV-CRF. In conclusion, central administration of CRF in neonatal chicks induces tissue speci fi c oxidative damage: higher MDA levels were observed in theheart and liver while no such change occurred in the brain and muscle.© 2008 Elsevier Inc. All rights reserved. 1. Introduction Regulation of energy homeostasis is an important function of thecentral nervous system (CNS) requiring adaptive responses to maintainand support life. Many central factors in fl uence this regulation that isvitalforhabituation,thermogenesis,andmetabolism.Amajorupstreamdeterminate of theseresponsesiscorticotropin-releasingfactor(CRF), a41-aminoacidpeptidehormoneproducedinthehypothalamus.CRFhasmultiple biological effects and plays a central regulatory role in thehypothalamic – pituitary – adrenal (HPA) axis. CRF rapidly mobilizes theorganisminresponsetostressorsandalsostimulatestheCNStorespondto environmental challenges. The CRF family of peptides is capable of strong anorectic and thermogenic effects, and plays a role in theregulation of energy balance (Richard et al., 2002).In mammals, central administration of CRF elevates sympatheticout fl ow (Brown et al., 1982a), sympathetic nerve activity to brownadipose tissue (Egawa et al., 1990), catecholamines (Brown et al., 1982a; Dunn and Berridge, 1987), and corticosterone (Brown et al.,1982b). Additionally, intracerebroventricular (ICV) infusion of urocor-tin (member of CRF family) or CRF increases whole body O 2 consumption and colonic temperature (de Fanti and Martinez, 2002).In neonatal chicks, CRF has been reported to activate HPA responses(Furuse et al., 1997). The activation of the HPA axis plays a role inthermogenesis of neonatal chicks: central administration of CRF-induced hyperthermia (Tachibana et al., 2004; Mujahid and Furuse,2008a), and dose-dependently increased O 2  consumption, CO 2  andheatproduction (Tachibanaet al.,2006). We have recentlyshown thatICV-CRF induces hyperthermia in neonatal chicks and increases thegene transcripts of enzymes involved in mitochondrial FA transportand oxidation, and subsequentlythe FA oxidation enzyme activities ina tissue speci fi c manner along with higher levels of plasma NEFA(Mujahid and Furuse, 2008a). Thus, the CRF-induced increasedexpression and activity of mitochondrial FA transport and oxidationenzymes, and associated hyperthermia may expose the tissues tooxidativestress: hyperthermiaand increasedexpression of mitochon-drial FA transport and oxidation enzymes were observed in heat-stressed chickens with enhanced reactive oxygen species productionand oxidative damage (Mujahid et al., 2005, 2006, 2007a,b).The ICV route of administration is used commonly to assess centraleffectsofneuropeptides.Toourknowledge,theeffectofICV-CRFtoexert Comparative Biochemistry and Physiology, Part A 151 (2008) 664 – 669  Abbreviations:  3HADH, 3-hydroxyacyl CoA dehydrogenase; AD, Alzheimer's disease;CNS, central nervous system; CPT-I, carnitine-palmitoyl-transferase-I; CPT-II, carnitine-palmitoyl-transferase-II;CS,citratesynthase;CRF,corticotropin-releasingfactor;EB,evansblue; FA, fatty acid; HPA, hypothalamic – pituitary – adrenal; ICV, intracerebroventricular;LCAD, long-chain acyl CoA dehydrogenase; MDA, malondialdehyde; NEFA, non-esteri fi edfatty acid; TBARS, thiobarbituric acid reactive substances; ROS, reactive oxygen species. ⁎  Corresponding author. Tel./fax: +81 92 642 2953. E-mail address:  ahmad@brs.kyushu-u.ac.jp (A. Mujahid).1095-6433/$  –  see front matter © 2008 Elsevier Inc. All rights reserved.doi:10.1016/j.cbpa.2008.08.013 Contents lists available at ScienceDirect Comparative Biochemistry and Physiology, Part A  journal homepage: www.elsevier.com/locate/cbpa  oxidative damage in the brain and other tissues has not been testedexplicitly. Therefore,inthepresentstudy we investigated whether ICV-CRF induces oxidative damage in the plasma and different tissues of neonatal chicks. We, measured malondialdehyde (MDA) levels in thebrain, heart and muscle, and also studied the gene transcripts of enzymes involved in mitochondrial FA transport and oxidation in thebrain with and without ICV-CRF. 2. Materials and methods  2.1. Animals and experimental design Layer-type (Julia) 1-day-old male chicks ( Gallus gallus ) wereobtained from a commercial hatchery (Murata Hatchery, Fukuoka, Japan). The chicks were housed in individual cages at a constanttemperature of 30±1 °C under continuous light and with  ad libitum access to water and commercial starter diet (Toyohashi Feed Mills CoLtd. Aichi, Japan). At 2 days, chicks ( n =6) were given ICV injection of CRF in Evans Blue (EB) saline solution or only EB saline solution andwere kept at thermoneutral temperature, 30 °C for 3 h. Chicks wereprovided adlibitum accesstofeedandwater.Bloodwascollectedfromthe jugular vein using a heparinized syringe immediately after 3 h of ICVinjection.Thereafter,chickswerekilledbycervicaldislocationandtheir tissues were rapidly excised. Tissues were frozen in liquidnitrogen and powdered, and then stored at  − 80 °C until required forfurther analysis. Experimental procedures followed the guidelines forAnimalExperimentsintheFacultyofAgriculture ofKyushuUniversityand the Law (No. 105) and Noti fi cation (No. 6) of the JapaneseGovernment. All efforts were made to minimize pain or discomfort of the animals used and to minimize the animal number.  2.2. ICV injection CRF (Peptide Institute, Osaka, Japan) was dissolved in 0.1% EB salinesolution and given as a 10  μ  L (42 pmol) ICV injection according to themethod of  Davis et al. (1979). The control group was injected with anequal volume of EB saline solution. The injection method has beenshown to cause no stress on chicks: ICV injection of 0.1% EB salinesolution has no effect on feeding behavior (Furuse et al., 1999) orcorticosterone release (Saito et al., 2005) when compared with intactchicks without injections. After sacri fi ce, con fi rmation of drug injectionwas carried out by observing the presence of EB dye in the lateralventricle. The results obtained from chicks with an insuf  fi cient amountor absences of EB dye in the lateral ventricle were excluded.  2.3. Plasma and tissue MDA Blood plasma and tissues (brain, liver, heart, and gastrocnemiusmuscle) were used for MDA measurements.Tissueswere homogenizedin a buffer (100 mM KCl, 50 mM Tris – HCl and 2 mM EGTA, pH 7.4),centrifuged at 700  g   and supernatant was collected. Plasma was col-lected by centrifuging blood samples at 700  g   for 10 min. Lipid pe-roxidation was determined colorimetrically as a 2-thiobarbituric acidreactive substance (TBARS) as described previously (Mujahid et al.,2007b).Brie fl y,tissuehomogenateorplasmasamplesweremixedwith8.1% SDS, 20% acetic acid (pH 3.5), 0.8% 2-thiobarbituric acid and 0.8%butyl-hydroxyltoluene.Aftervortexing,sampleswereincubatedfor1hon ice andthenat95 °Cfor 1 h before beingtransferredto ice. Butanol-pyridine 15:1 (v/v) was added, the samples were then mixed byvortexing and centrifuged at 1000  g   for 10 min. Absorbance of thesupernatant, consisting of the butanol-pyridine layer, was measured at532 nm. The content of TBARS is expressed as the MDA equivalent. Theprotein content of tissue homogenates was determined by thebicinchoninic acid assay with bovine serum albumin as the standardandMDAcontentswereexpressedaspermgprotein.Thesampleswereanalyzed within 1 week of storage at  − 80 °C.  2.4. Quanti  fi cation of mRNA using real-time RT-PCR Standard molecular biological techniques were used, essentially asdescribedbySambrooketal.(1989).TissueswerehomogenizedinTrizol-Reagent (Invitrogen, San Diego, CA, USA) and total RNA was isolatedaccording to the manufacturer's protocol. To study progressive altera-tionsintheexpressionoftargetgenes,thatis,mitochondrialFAtransportand oxidation-related genes [carnitine-palmitoyl-transferase-I (CPT-I),carnitine-palmitoyl-transferase-II(CPT-II),long-chainacylCoAdehydro-genase (LCAD), 3-hydroxyacyl CoA dehydrogenase (3HADH) and citratesynthase (CS)], real-time reverse transcription-polymerase chain reac-tion (RT-PCR) analysis was performed using the iCycler Real TimeDetection System (Bio-Rad Laboratories, Hercules, CA, USA). Five µg of  Fig. 1.  Weight gain (A) and feed consumption (B) of neonatal chicks with or withoutintracerebroventricular injection of corticotropin-releasing factor (CRF). Values aremeans±S.E. of six chicks.  ⁎ P  b 0.05 for saline group vs. CRF group. Fig. 2.  Plasma malondialdehyde (MDA) levels of neonatal chicks with or withoutintracerebroventricular injection of corticotropin-releasing factor (CRF). Values aremeans±S.E. of six chicks.  ⁎ P  b 0.05 for saline group vs. CRF group.665  A. Mujahid, M. Furuse / Comparative Biochemistry and Physiology, Part A 151 (2008) 664 – 669  totalRNA,prepared usingTrizol-Reagent, wasreverse transcribedusinga mixture of oligo(dT) 12 – 18 and random primers, and M-MLV reversetranscriptase (Invitrogen, San Diego, CA, USA). One µL of each reversetranscription reactionproductthen served as a template in a 50- μ  L PCR reaction containing 2 mM MgCl 2 , 0.5  μ  M of each primer and 0.5× SYBR Greenmastermix(BioWhittakerMolecularApplications,Rockland,ME,USA).TheSYBRGreen fl uorescencewasdetectedattheendofeachcycleto monitor the amount of PCR product formed during that cycle. At theend of each run, melting curve pro fi les were recorded. Oligonucleotidesequences of sense and antisense primers and annealing temperatureswere the same as described previously (Mujahid et al., 2007a). Thespeci fi city of the ampli fi cation product was further veri fi ed byelectrophoresis on a 0.8% agarose gel and by DNA sequencing. ResultsarepresentedastheratioofmRNAto18SrRNAtocorrectfordifferencesin the amounts of template cDNA used.  2.5. 3HADH and CS activity 3HADH and CS activities were measured according tothe methodsof  Bradshaw and Noyes (1975) and Srere (1969), respectively.  2.6. Statistical analysis Data were analyzed using the Statistical Analysis System (Cary, NC,USA). Statistical signi fi cance of the difference was determined usingStudent's  t  -test for comparison of results from control and centrallyadministered CRF groups. All data are expressed as means±standarderror(S.E.).Differenceswereconsideredsigni fi cantforvaluesof  P  b 0.05. 3. Results  3.1. Body weight change and feed consumption As shown in Fig.1A, loss in body weight was observed in neonatalchicks with ICV-CRF ( P  b 0.0001). Feed consumption (Fig. 1B) of neonatalchickswithICV-CRFwassigni fi cantlydecreasedascomparedto that of control chicks ( P  b 0.0001).  3.2. Plasma oxidative damage To study oxidative damage to plasma, MDA, an oxidative stressbiomarker for peroxidized lipids was measured. Neonatal chicks withICV-CRF showed signi fi cantly higher plasma MDA levels as comparedto that of control chicks (Fig. 2,  P  b 0.001).  3.3. Tissue oxidative damage As shown in Fig. 3A – D, MDA levels in neonatal chicks with ICV-CRFwere higher in heart and liver ( P  b 0.001), while no such change wasobserved in brain and skeletal muscle (gastrocnemius), as compared tothat of control chicks.  3.4. Gene transcripts for mitochondrial FA transport and oxidationenzymes Gene expression of the mitochondrial FA transport and oxidation-related enzymes (CPT-1, CPT-II, LCAD,3HADH and CS) was analyzed inthe brain by real-time RT-PCR analysis (Fig. 4A). Gene transcripts of these enzymes did not change in neonatal chicks with ICV-CRF ascompared to that of control chicks.  3.5. Enzyme activity Activities of 3HADH and CS enzymes did not change in the brain of neonatalchickswithICV-CRFascomparedtothatofcontrolchicks(Fig.4B). 4. Discussion CRF is a neuropeptide with multiple biological effects and plays acentral regulatory role to modulate the activity of the HPA axis. CRF Fig.3. Malondialdehyde(MDA)levelsinthebrain(A),heart(B),liver(C),andskeletalmuscle(D)ofneonatalchickswithorwithoutintracerebroventricularinjectionofcorticotropin-releasing factor (CRF). Values are means±S.E. of six chicks.  ⁎ P  b 0.05 for saline group vs. CRF group.666  A. Mujahid, M. Furuse / Comparative Biochemistry and Physiology, Part A 151 (2008) 664 – 669  mediates neuroendocrine modulations in response to stressfulstimuli. In the present study, we con fi rmed that centrally adminis-teredCRFdecreasedfoodintakeofneonatalchicks.Previousstudiesinour laboratory showed that CRF-induced decrease in food intake wasdose-dependent and chicks treated with CRF ate feed within  fi rst30 min, but thereafter did not eat any more. The studies indicatedthat food intake was not completely inhibited by CRF immediatelyafter ICV injection, but the inhibitionwas detectable after 30 min andcontinued for at least 2 h after injection (Furuse et al., 1997; Ohgushiet al., 2001; Zhang et al., 2001). Our present study further extendsthese  fi ndings that the CRF-induced anorexia was prolonged for atleast 3 h. These  fi ndings indicate that central CRF is the potent in-hibitor of food intake in the chicks.Central administration of CRF in neonatal chicks increases the coretemperature that is associated with enhanced gene transcripts of mitochondrial FA transport and oxidation enzymes in the liver andheart (Mujahid and Furuse, 2008a,b). CRF rapidly mobilizes theorganism in response to stressors and provokes physiologicalmodulations related to oxygen consumption, and induces changes inCO 2  and energy production (Tachibana et al., 2006). Subsequently,these changes may result in increased reactive oxygen species (ROS)production and a state of oxidative stress leading to oxidative damageand impairment of cellular homeostasis: lipid peroxidation resultsfrom reactions between ROS and polyunsaturated fatty acids of cellmembranes as a result of oxidative stress and markedly damages thestructure and function of cell membranes invarious tissues (Halliwell,1992).We therefore, studied the effect of centrally administered CRF onthe oxidative damage in the plasma, brain and other tissues: theamount of lipid peroxidation product is used as an index of oxidativestress (Sies, 1986). Of the many biological targets of oxidative stress,lipids are the most common and MDA is the principal product of polyunsaturated fatty acid peroxidation. We measured MDA in dif-ferent tissues as an index of oxidative damage. These tissues wereselected owing to their respective roles in lipid assimilation (liver), asa major oxidation site (heart and muscle), and as a sitewith enhancedlevels of easily peroxidizable long-chain polyunsaturates for function(brain) that is not particularly enriched in protective antioxidantenzymes or other antioxidant compounds (Beckman 1991; Jain et al.,1991). Results of the present study revealed that central administra-tion of CRF signi fi cantly increased plasma MDA levels that indicated astate of systemic oxidative stress by ICV-CRF. Therefore, we furtherstudied different organs in details and found higher MDA levels in theheart and liverof ICV-CRF neonatal chicks compared tothat of controlchicks. In contrast to this, no increase in MDA levels was observed inthe brain and muscle.We have previously shown that ICV-CRF increases the plasmaNEFA levels and gene transcripts of CPT-I and II, 3HADH, LCAD and CSin the liver and heart while no such change occurs in skeletal muscle(Mujahid and Furuse, 2008a). In this study we hypothesized that Fig. 4.  Gene expression (A) and enzyme activities (B) in the brain of neonatal chicks with or without intracerebroventricular injection of corticotropin-releasing factor (CRF). Real-time RT-PCR was performed to determine gene expression of CPT-I, CPT-II, LCAD, 3HADH and CS transcripts in the brain of neonatal chicks. Results were normalized to 18S rRNAtranscript levels. Values are means±S.E. of six chicks.667  A. Mujahid, M. Furuse / Comparative Biochemistry and Physiology, Part A 151 (2008) 664 – 669  possible enhancement in CRF-induced substrate oxidation andassociatedhyperthermiamightbeassociatedwithincreasedoxidativedamage. Results of the present study con fi rmed this hypothesis: theliver and heart that have been previously shown to increase themitochondrial FA transport and oxidation by ICV-CRF, in the presentstudyshowedincreasedoxidative damage. In contrast tothis,ICV-CRFthat previously exhibited no change in gene transcripts of skeletalmuscle mitochondrial FA transport and oxidation enzymes (Mujahidand Furuse, 2008a), in the present study also showed no change inoxidativedamage.Inthepresentexperiment,wealsostudiedthegenetranscripts and enzyme activities of mitochondrial FA oxidationenzymes in the brain, and found no difference between control andICV-CRF chicks. Thus, the MDA levels in different tissues seem to bedirectly related with the state of mitochondrial substrate oxidation inCRF-administered neonatal chicks.With regard to metabolic changes, maintenance of energy home-ostasis is governed by the brain. Afferent signals indicating the energystatus of the animal and the state of its external environment, in-cluding the presence of physiological and/or psychological stressors,are integrated centrally. Thus, the efferent pathways controllingbehavior and energy expenditure are modulated accordingly. Thecore site of these integrative processes is the hypothalamus, where anarray of neurotransmitters, including many neuropeptides, modula-tes signals through complex neural circuits (Dallman et al., 2006).Cardiovascular function is regulated by both neural and hormonalefferent mechanisms of the CNS. CRF acts within the CNS to stimulatesympathetic nervous out fl ow, and a local increase of CRF in thepreoptic area and dorsomedial sites of the hypothalamus results inincreased heart rate (Fisher et al., 1983; Cerri and Morrison, 2006).Central administration of CRF in neonatal chicks strongly in fl uencestheheartthatrespondsbysigni fi cantincreaseinoxidativemetabolismas compared tothatof skeletal muscle (Mujahid and Furuse, 2008a,b).This CRF-induced increased oxidative metabolism (Mujahid andFuruse, 2008a,b) and increased heart rate (Fisher et al., 1983; Cerriand Morrison, 2006) might be responsible for increased oxidativedamageintheheartasobservedinthepresentstudy.Skeletalmusclesin neonatal chicks on the other hand might not be stimulated tomodulate oxidative metabolism by central administration of CRF orlow environmental temperature exposure (Mujahid and Furuse,2008a,b). CRF can directly stimulate thermogenesis in intact mouseskeletal muscle and this direct action of CRF may be mediated bysubstrate cycling between de novo lipogenesis and lipid oxidation,orchestrated by phosphatidylinositol 3-kinase and AMP-activatedprotein kinase signaling (Solinas et al., 2006). However, this is notthe case in the physiological state, since the peripheral concentrationof CRF is negligible. The different response of skeletal muscle inneonatalchickstocentraladministrationofCRFascomparedtothatof the heart may be due to distinct neural and hormonal efferentmechanisms,stateofmusclematurityandfunction,thresholdlevelsof oxidants, antioxidantcapacityor some otherfactor(s) that needs to beelucidated in order to investigate the patho-physiological mechanismof stress.CRF may act as an endogenous neuroprotective hormone duringconditions of oxidative stress. CRF provides moderate protection tohypoxic hippocampal neurons in the brain slice preparations thatappears to be a direct neuronal effect (Fox et al., 1993). In primaryneuronal culture, CRF protects neurons against lipid peroxidation-induced death (Pedersen et al., 2001). Evidence for neuroprotectiveactions of CRF is strengthened by the observations that signi fi cantchanges in CRF concentrations are present in animal model studies of Alzheimer's disease (AD) as well as in patients suffering from AD.Speci fi cally, reductions in brain tissue CRF concentration have beendetected in the frontal and temporal cortex (Bissette et al., 1985;Whitehouse et al., 1987). A correlation between CSF-CRF levels andglobal neuropsychological impairment ratings has been shown, sug-gesting that greater cognitive impairment was associated with lowerCSF-CRF concentrations (Pomara et al., 1989). Furthermore, CRF-immunopositive neurons are pathologically altered in AD diseasedbrains and abnormal CRF-immunoreactive axons as well as neuritesassociated with deposits of amyloid in brain regions showing senileplaqueshavebeenidenti fi ed.ThenumberofCRF-immunoreactive fi bersis decreased in individuals with AD (Bissette et al.,1985; Powers et al.,1987).ThesestudiesindicatedthatCRFcouldplayaneuroprotectiverolein patho-physiological conditions characterized by oxidative stress. Inthepresentstudy,MDAlevelsinthebrainofcentrallyadministeredCRFchicks were unchanged.Chicks with ICV-CRFalsoshowed nochange ingene transcripts of mitochondrial FA transport and oxidation enzymes,andactivitiesofFAoxidationenzymesinthebrain(Fig.4).Therefore,theCRF in theCNS seems toplaya neuroprotective role in thebrainagainstoxidative damage associated with patho-physiological condition(s)where oxidative stress is high, while no such effect is seen undernormal physiological conditions, a hypothesis that needs to be elu-cidated in future studies.Inconclusion,centraladministrationofCRFinneonatalchicksinducestissuespeci fi coxidativedamage:higherMDAlevelswereobservedintheheart and liver, while no such changes occurred in the brain and muscle.This study provides  fi rst evidence that ICV-CRF induces enhancement of plasma MDA and causes tissue speci fi c oxidative damage.  Acknowledgements This work was supported by a Grant-in-Aid for Japan Society forthe Promotion of Science (JSPS) Postdoctoral Fellowship for ForeignResearchers to M.A. (No.197179) and a Grant-in-Aid for Scienti fi cResearch from JSPS to M.F. (No. 18208023). References Beckman, J.S., 1991. The double-edged role of nitric oxide in brain function andsuperoxide-mediated injury. J. Dev. Physiol.15, 53 – 59.Bissette, G., Reynolds, G.P., Kilts, C.D., Widerlov, E., Nemeroff, C.B., 1985. Corticotropin-releasing factor-like immunoreactivity in senile dementia of the Alzheimer typereduced cortical and striatal concentrations. JAMA 254, 3067 – 3069.Bradshaw, R.A., Noyes, B.E.,1975.  L  -3-hydroxyacyl coenzyme A dehydrogenase from pigheart muscle. EC 1.1.1.35  L  -3-hydroxyacyl CoA: NAD oxidoreductase. MethodsEnzymol. 35,122 – 128.Brown, M.R., Fisher, L.A., Rivier, J., Spiess, J., Rivier, C., Vale, W., 1982a. Corticotropin-releasing factor: effects on the sympathetic nervous system and oxygen consump-tion. Life Sci. 30, 207 – 210.Brown, M.R.,Fisher,L.A., Spiess, J., Rivier,J., Rivier,C., Vale, W.,1982b. Comparison of thebiologic actions of corticotropin-releasing factor and sauvagine. Regul. Pept. 4,107 – 114.Cerri,M.,Morrison,S.F.,2006.Corticotropin-releasingfactorincreasesinbrownadiposetissue thermogenesis and heart rate through dorsomedial hypothalamus andmedullary raphe pallidus. Neuroscience 140, 711 – 721.Dallman, M.F., Pecoraro, N.C., La Fleur, S.E., Warne, J.P., Ginsberg, A.B., Akana, S.F.,Laugero, K.C., Houshyar, H., Strack, A.M., Bhatnagar, S., Bell, M.E., 2006.Glucocorticoids, chronic stress, and obesity. Prog. Brain Res. 153, 75 – 105.Davis, J.L., Masuoka, D.T., Gerbrandt, L.K., Cherkin, A., 1979. Autoradiographicdistribution of   L  -proline in chicks after intracerebral injection. Physiol. Behav. 22,693 – 695.deFanti,B.A.,Martinez,J.A.,2002.Centralurocortinactivationofsympathetic-regulatedenergy metabolism in Wistar rats. Brain Res. 930, 37 – 41.Dunn, A.J., Berridge, C.W., 1987. Corticotropin-releasing factor administration elicits astress-like activation of cerebral catecholaminergic systems. Pharmacol. Biochem.Behav. 27, 685 – 691.Egawa, M., Yoshimatsu, H., Bray, G.A., 1990. Preoptic area injection of corticotropin-releasing hormone stimulates sympathetic activity.Am. J. Physiol.259, R799 – R806.Fisher, L.A., Jessen, G., Brown, M.R., 1983. Corticotropin-releasing factor (CRF):mechanismtoelevatemeanarterialpressureandheartrate.Regul.Pept.5,153 – 161.Fox, M.W., Anderson, R.E., Meyer, F.B.,1993. Neuroprotection bycorticotropin-releasingfactor during hypoxia in rat brain. Stroke 24,1072 – 1076.Furuse, M., Ando, R., Bungo, T., Ao, R., Shimojo, M., Masuda, Y., 1999. Intracerebroven-tricular injection of orexins does not stimulate food intake in neonatal chicks. Br.Poult. Sci. 40, 698 – 700.Furuse, M., Matsumoto, M., Saito, N., Sugahara, K., Hasegawa, S., 1997. The centralcorticotropin-releasing factor and glucagon-like peptide-1 in food intake of theneonatal chick. Eur. J. Pharmacol. 339, 211 – 214.Halliwell, B., 1992. Reactive oxygen species and the central nervous system. J. Neurochem. 59, 1609 – 1623. Jain, A.,Martensson,J.,Stole,E., Auld, P.A.,Meister,A.,1991.Glutathione de fi ciencyleadsto mitochondrial damage in brain. Proc. Natl. Acad. Sci. USA 88, 1913 – 1917.668  A. Mujahid, M. Furuse / Comparative Biochemistry and Physiology, Part A 151 (2008) 664 – 669
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