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[PMID]: 25813907
[Au] Autor:Gutierrez-Aguilar R; Thompson A; Marchand N; Dumont P; Woods SC; de Launoit Y; Seeley RJ; Ulrich-Lai YM
[Ad] Address:Department of Internal Medicine, University of Cincinnati, United States; Laboratorio de Enfermedades Metabólicas Obesidad y Diabetes, Hospital Infantil de México Federico Gómez, Mexico. Electronic address: ruthgutierrezhimfg@gmail.com....
[Ti] Title:The obesity-associated transcription factor ETV5 modulates circulating glucocorticoids.
[So] Source:Physiol Behav;150:38-42, 2015 Oct 15.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The transcription factor E-twenty-six version 5 (ETV5) has been linked with obesity in genome-wide association studies. Moreover, ETV5-deficient mice (knockout; KO) have reduced body weight, lower fat mass, and are resistant to diet-induced obesity, directly linking ETV5 to the regulation of energy balance and metabolism. ETV5 is expressed in hypothalamic brain regions that regulate both metabolism and HPA axis activity, suggesting that ETV5 may also modulate HPA axis function. In order to test this possibility, plasma corticosterone levels were measured in ETV5 KO and wildtype (WT) mice before (pre-stress) and after (post-stress) a mild stressor (intraperitoneal injection). ETV5 deficiency increased both pre- and post-stress plasma corticosterone, suggesting that loss of ETV5 elevated glucocorticoid tone. Consistent with this idea, ETV5 KO mice have reduced thymus weight, suggestive of increased glucocorticoid-induced thymic involution. ETV5 deficiency also decreased the mRNA expression of glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and vasopressin receptor 1A in the hypothalamus, without altering vasopressin, corticotropin-releasing hormone, or oxytocin mRNA expression. In order to test whether reduced MR and GR expression affected glucocorticoid negative feedback, a dexamethasone suppression test was performed. Dexamethasone reduced plasma corticosterone in both ETV5 KO and WT mice, suggesting that glucocorticoid negative feedback was unaltered by ETV5 deficiency. In summary, these data suggest that the obesity-associated transcription factor ETV5 normally acts to diminish circulating glucocorticoids. This might occur directly via ETV5 actions on HPA-regulatory brain circuitry, and/or indirectly via ETV5-induced alterations in metabolic factors that then influence the HPA axis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 1296991 MEDLINE  
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[PMID]: 25747321
[Au] Autor:Egan AE; Ulrich-Lai YM
[Ad] Address:Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati School of Medicine, Cincinnati, OH, 45237, USA; Neuroscience Graduate Program, University of Cincinnati School of Medicine, Cincinnati, OH, 45237, USA.
[Ti] Title:Activation of physiological stress responses by a natural reward: Novel vs. repeated sucrose intake.
[So] Source:Physiol Behav;150:43-52, 2015 Oct 15.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pharmacological rewards, such as drugs of abuse, evoke physiological stress responses, including increased heart rate and blood pressure, and activation of the hypothalamic-pituitary-adrenal (HPA) axis. It is not clear to what extent the natural reward of palatable foods elicits similar physiological responses. In order to address this question, HPA axis hormones, heart rate, blood pressure and brain pCREB immunolabeling were assessed following novel and repeated sucrose exposure. Briefly, adult, male rats with ad libitum food and water were given either a single (day 1) or repeated (twice-daily for 14days) brief (up to 30min) exposure to a second drink bottle containing 4ml of 30% sucrose drink vs. water (as a control for bottle presentation). Sucrose-fed rats drank more than water-fed on all days of exposure, as expected. On day 1 of exposure, heart rate, blood pressure, plasma corticosterone, and locomotion were markedly increased by presentation of the second drink bottle regardless of drink type. After repeated exposure (day 14), these responses habituated to similar extents regardless of drink type and pCREB immunolabeling in the hypothalamic paraventricular nucleus (PVN) also did not vary with drink type, whereas basolateral amygdala pCREB was increased by sucrose intake. Taken together, these data suggest that while sucrose is highly palatable, physiological stress responses were evoked principally by the drink presentation itself (e.g., an unfamiliar intervention by the investigators), as opposed to the palatability of the offered drink.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  3 / 1296991 MEDLINE  
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[PMID]: 25666308
[Au] Autor:Panagiotakopoulos L; Kelly S; Neigh GN
[Ad] Address:Department of Pediatrics, Division of Pediatric Endocrinology, Emory University, United States.
[Ti] Title:HIV-1 proteins accelerate HPA axis habituation in female rats.
[So] Source:Physiol Behav;150:8-15, 2015 Oct 15.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Congenital infection by the Human Immunodeficiency Virus (HIV) has been shown to lead to multiple co-morbidities, and people living with HIV have a higher incidence of affective and anxiety disorders. A marked increase in mood disorders is evident during the sensitive phase of adolescence and this is further pronounced in females. Depression has been linked to dysfunction of the intracellular response system to corticosteroids at the level of the hippocampus (HC) and prefrontal cortex (PFC) with a notable role of the glucocorticoid receptor (GR) and its co-chaperones (FKBP5 and FKBP4). The current study examined the extent to which HIV protein expression in adolescent female rats altered the stress response at both the level of corticosterone output and molecular regulation of the glucocorticoid receptor in the brain. WT and HIV-1 genotype female rats were randomly allocated in control, acute stress and repeat stress groups. Corticosterone plasma levels and expression of GR, FKBP4, and FKBP5 in the HC and PFC were measured. The presence of HIV-1 proteins facilitates habituation of the corticosterone response to repeated stressors, such that HIV-1 TG rats habituated to repeated restraint and WT rats did not. This was reflected by interactions between stress exposure and HIV-1 protein expression at the level of GR co-chaperones. Although expression of the GR was similarly reduced after acute and repeat stress in both genotypes, expression of FKBP5 and FKBP4 was altered in a brain-region specific manner depending on the duration of the stress exposure and the presence or absence of HIV-1 proteins. Collectively, the data presented demonstrate that HIV-1 proteins accelerate habituation to repeated stressors and modify the influence of acute and repeat stressors on GR co-chaperones in a brain region-specific manner.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 1296991 MEDLINE  
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[PMID]: 25510640
[Au] Autor:McDonald CJ; Acheff E; Kennedy R; Taylor L; Curthoys NP
[Ad] Address:Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523-1870, United States....
[Ti] Title:Effect of lysine to alanine mutations on the phosphate activation and BPTES inhibition of glutaminase.
[So] Source:Neurochem Int;88:10-4, 2015 Sep.
[Is] ISSN:1872-9754
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The GLS1 gene encodes a mitochondrial glutaminase that is highly expressed in brain, kidney, small intestine and many transformed cells. Recent studies have identified multiple lysine residues in glutaminase that are sites of N-acetylation. Interestingly, these sites are located within either a loop segment that regulates access of glutamine to the active site or the dimer:dimer interface that participates in the phosphate-dependent oligomerization and activation of the enzyme. These two segments also contain the binding sites for bis-2[5-phenylacetamido-1,2,4-thiadiazol-2-yl]ethylsulfide (BPTES), a highly specific and potent uncompetitive inhibitor of this glutaminase. BPTES is also the lead compound for development of novel cancer chemotherapeutic agents. To provide a preliminary assessment of the potential effects of N-acetylation, the corresponding lysine to alanine mutations were constructed in the hGACΔ1 plasmid. The wild type and mutated proteins were purified by Ni(+)-affinity chromatography and their phosphate activation and BPTES inhibition profiles were analyzed. Two of the alanine substitutions in the loop segment (K311A and K328A) and the one in the dimer:dimer interface (K396A) form enzymes that require greater concentrations of phosphate to produce half-maximal activation and exhibit greater sensitivity to BPTES inhibition. By contrast, the K320A mutation results in a glutaminase that exhibits near maximal activity in the absence of phosphate and is not inhibited by BPTES. Thus, lysine N-acetylation may contribute to the acute regulation of glutaminase activity in various tissues and alter the efficacy of BPTES-type inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 1296991 MEDLINE  
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[PMID]: 25128239
[Au] Autor:Karki P; Smith K; Johnson J; Aschner M; Lee E
[Ad] Address:Department of Physiology, Meharry Medical College, Nashville, TN 37208, United States....
[Ti] Title:Role of transcription factor yin yang 1 in manganese-induced reduction of astrocytic glutamate transporters: Putative mechanism for manganese-induced neurotoxicity.
[So] Source:Neurochem Int;88:53-9, 2015 Sep.
[Is] ISSN:1872-9754
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Astrocytes are the most abundant non-neuronal glial cells in the brain. Once relegated to a mere supportive role for neurons, contemporary dogmas ascribe multiple active roles for these cells in central nervous system (CNS) function, including maintenance of optimal glutamate levels in synapses. Regulation of glutamate levels in the synaptic cleft is crucial for preventing excitotoxic neuronal injury. Glutamate levels are regulated predominantly by two astrocytic glutamate transporters, glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST). Indeed, the dysregulation of these transporters has been linked to several neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD), as well as manganism, which is caused by overexposure to the trace metal, manganese (Mn). Although Mn is an essential trace element, its excessive accumulation in the brain as a result of chronic occupational or environmental exposures induces a neurological disorder referred to as manganism, which shares common pathological features with Parkinsonism. Mn decreases the expression and function of both GLAST and GLT-1. Astrocytes are commonly targeted by Mn, and thus reduction in astrocytic glutamate transporter function represents a critical mechanism of Mn-induced neurotoxicity. In this review, we will discuss the role of astrocytic glutamate transporters in neurodegenerative diseases and Mn-induced neurotoxicity.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 1296991 MEDLINE  
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[PMID]: 26026616
[Au] Autor:Stengel A; Karasawa H; Taché Y
[Ad] Address:Charité Center for Internal Medicine and Dermatology, Division of General Internal and Psychosomatic Medicine, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
[Ti] Title:The role of brain somatostatin receptor 2 in the regulation of feeding and drinking behavior.
[So] Source:Horm Behav;73:15-22, 2015 Jul.
[Is] ISSN:1095-6867
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Somatostatin was discovered four decades ago as hypothalamic factor inhibiting growth hormone release. Subsequently, somatostatin was found to be widely distributed throughout the brain and to exert pleiotropic actions via interaction with five somatostatin receptors (sst1-5) that are also widely expressed throughout the brain. Interestingly, in contrast to the predominantly inhibitory actions of peripheral somatostatin, the activation of brain sst2 signaling by intracerebroventricular injection of stable somatostatin agonists potently stimulates food intake and independently, drinking behavior in rodents. The orexigenic response involves downstream orexin-1, neuropeptide Y1 and µ receptor signaling while the dipsogenic effect is mediated through the activation of the brain angiotensin 1 receptor. Brain sst2 activation is part of mechanisms underlying the stimulation of feeding and more prominently water intake in the dark phase and is able to counteract the anorexic response to visceral stressors.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 1296991 MEDLINE  
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[PMID]: 26012711
[Au] Autor:Model Z; Butler MP; LeSauter J; Silver R
[Ad] Address:Department of Psychology, Barnard College, New York, NY, USA. Electronic address: model.zina@gmail.com....
[Ti] Title:Suprachiasmatic nucleus as the site of androgen action on circadian rhythms.
[So] Source:Horm Behav;73:1-7, 2015 Jul.
[Is] ISSN:1095-6867
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Androgens act widely in the body in both central and peripheral sites. Prior studies indicate that in the mouse, suprachiasmatic nucleus (SCN) cells bear androgen receptors (ARs). The SCN of the hypothalamus in mammals is the locus of a brain clock that regulates circadian rhythms in physiology and behavior. Gonadectomy results in reduced AR expression in the SCN and in marked lengthening of the period of free-running activity rhythms. Both responses are restored by systemic administration of androgens, but the site of action remains unknown. Our goal was to determine whether intracranial androgen implants targeted to the SCN are sufficient to restore the characteristic free-running period in gonadectomized male mice. The results indicate that hypothalamic implants of testosterone propionate in or very near the SCN produce both anatomical and behavioral effects, namely increased AR expression in the SCN and restored period of free-running locomotor activity. The effect of the implant on the period of the free-running locomotor rhythm is positively correlated with the amount of AR expression in the SCN. There is no such correlation of period change with amount of AR expression in other brain regions examined, namely the preoptic area, bed nucleus of the stria terminalis and premammillary nucleus. We conclude that the SCN is the site of action of androgen effects on the period of circadian activity rhythmicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 1296991 MEDLINE  
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[PMID]: 25863357
[Au] Autor:Foote M; Qiao H; Graham K; Wu Y; Zhou Y
[Ad] Address:Department of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, Florida....
[Ti] Title:Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice.
[So] Source:Biol Psychiatry;78(6):386-95, 2015 Sep 15.
[Is] ISSN:1873-2402
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The 14-3-3 family of proteins is implicated in the regulation of several key neuronal processes. Previous human and animal studies suggested an association between 14-3-3 dysregulation and schizophrenia. METHODS: We characterized behavioral and functional changes in transgenic mice that express an isoform-independent 14-3-3 inhibitor peptide in the brain. RESULTS: We recently showed that 14-3-3 functional knockout mice (FKO) exhibit impairments in associative learning and memory. We report here that these 14-3-3 FKO mice display other behavioral deficits that correspond to the core symptoms of schizophrenia. These behavioral deficits may be attributed to alterations in multiple neurotransmission systems in the 14-3-3 FKO mice. In particular, inhibition of 14-3-3 proteins results in a reduction of dendritic complexity and spine density in forebrain excitatory neurons, which may underlie the altered synaptic connectivity in the prefrontal cortical synapse of the 14-3-3 FKO mice. At the molecular level, this dendritic spine defect may stem from dysregulated actin dynamics secondary to a disruption of the 14-3-3-dependent regulation of phosphorylated cofilin. CONCLUSIONS: Collectively, our data provide a link between 14-3-3 dysfunction, synaptic alterations, and schizophrenia-associated behavioral deficits.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 1296991 MEDLINE  
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[PMID]: 25758057
[Au] Autor:Morishita H; Cabungcal JH; Chen Y; Do KQ; Hensch TK
[Ad] Address:FM Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts....
[Ti] Title:Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons.
[So] Source:Biol Psychiatry;78(6):396-402, 2015 Sep 15.
[Is] ISSN:1873-2402
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Oxidative stress and the specific impairment of perisomatic gamma-aminobutyric acid circuits are hallmarks of the schizophrenic brain and its animal models. Proper maturation of these fast-spiking inhibitory interneurons normally defines critical periods of experience-dependent cortical plasticity. METHODS: Here, we linked these processes by genetically inducing a redox dysregulation restricted to such parvalbumin-positive cells and examined the impact on critical period plasticity using the visual system as a model (3-6 mice/group). RESULTS: Oxidative stress was accompanied by a significant loss of perineuronal nets, which normally enwrap mature fast-spiking cells to limit adult plasticity. Accordingly, the neocortex remained plastic even beyond the peak of its natural critical period. These effects were not seen when redox dysregulation was targeted in excitatory principal cells. CONCLUSIONS: A cell-specific regulation of redox state thus balances plasticity and stability of cortical networks. Mistimed developmental trajectories of brain plasticity may underlie, in part, the pathophysiology of mental illness. Such prolonged developmental plasticity may, in turn, offer a therapeutic opportunity for cognitive interventions targeting brain plasticity in schizophrenia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review

  10 / 1296991 MEDLINE  
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[PMID]: 25758056
[Au] Autor:Bois C; Ronan L; Levita L; Whalley HC; Giles S; McIntosh AM; Fletcher PC; Owens DC; Johnstone EC; Lawrie SM
[Ad] Address:Division of Psychiatry, University of Edinburgh, Royal Edinburgh Hospital, Edinburgh, United Kingdom. Electronic address: C.bois@sms.ed.ac.uk....
[Ti] Title:Cortical Surface Area Differentiates Familial High Risk Individuals Who Go on to Develop Schizophrenia.
[So] Source:Biol Psychiatry;78(6):413-20, 2015 Sep 15.
[Is] ISSN:1873-2402
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Schizophrenia is associated with structural brain abnormalities that may be present before disease onset. It remains unclear whether these represent general vulnerability indicators or are associated with the clinical state itself. METHODS: To investigate this, structural brain scans were acquired at two time points (mean scan interval 1.87 years) in a cohort of individuals at high familial risk of schizophrenia (n = 142) and control subjects (n = 36). Cortical reconstructions were generated using FreeSurfer. The high-risk cohort was subdivided into individuals that remained well during the study, individuals that had transient psychotic symptoms, and individuals that subsequently became ill. Baseline measures and longitudinal change in global estimates of thickness and surface area and lobar values were compared, focusing on overall differences between high-risk individuals and control subjects and then on group differences within the high-risk cohort. RESULTS: Longitudinally, control subjects showed a significantly greater reduction in cortical surface area compared with the high-risk group. Within the high-risk group, differences in surface area at baseline predicted clinical course, with individuals that subsequently became ill having significantly larger surface area than individuals that remained well during the study. For thickness, longitudinal reductions were most prominent in the frontal, cingulate, and occipital lobes in all high-risk individuals compared with control subjects. CONCLUSIONS: Our results suggest that larger surface areas at baseline may be associated with mechanisms that go above and beyond a general familial disposition. A relative preservation over time of surface area, coupled with a thinning of the cortex compared with control subjects, may serve as vulnerability markers of schizophrenia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review


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