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[PMID]:28465284
[Au] Autor:Qian J; Thomas AP; Schroeder AM; Rakshit K; Colwell CS; Matveyenko AV
[Ad] Endereço:Departments of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California.
[Ti] Título:Development of diabetes does not alter behavioral and molecular circadian rhythms in a transgenic rat model of type 2 diabetes mellitus.
[So] Source:Am J Physiol Endocrinol Metab;313(2):E213-E221, 2017 08 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolic state and circadian clock function exhibit a complex bidirectional relationship. Circadian disruption increases propensity for metabolic dysfunction, whereas common metabolic disorders such as obesity and type 2 diabetes (T2DM) are associated with impaired circadian rhythms. Specifically, alterations in glucose availability and glucose metabolism have been shown to modulate clock gene expression and function in vitro; however, to date, it is unknown whether development of diabetes imparts deleterious effects on the suprachiasmatic nucleus (SCN) circadian clock and SCN-driven outputs in vivo. To address this question, we undertook studies in aged diabetic rats transgenic for human islet amyloid polypeptide, an established nonobese model of T2DM (HIP rat), which develops metabolic defects closely recapitulating those present in patients with T2DM. HIP rats were also cross-bred with a clock gene reporter rat model (Per1:luciferase transgenic rat) to permit assessment of the SCN and the peripheral molecular clock function ex vivo. Utilizing these animal models, we examined effects of diabetes on ) behavioral circadian rhythms, ) photic entrainment of circadian activity, ) SCN and peripheral tissue molecular clock function, and ) melatonin secretion. We report that circadian activity, light-induced entrainment, molecular clockwork, as well as melatonin secretion are preserved in the HIP rat model of T2DM. These results suggest that despite the well-characterized ability of glucose to modulate circadian clock gene expression acutely in vitro, SCN clock function and key behavioral and physiological outputs appear to be preserved under chronic diabetic conditions characteristic of nonobese T2DM.
[Mh] Termos MeSH primário: Comportamento Animal/fisiologia
Ritmo Circadiano/genética
Diabetes Mellitus Tipo 2
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Experimental/fisiopatologia
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Diabetes Mellitus Tipo 2/patologia
Diabetes Mellitus Tipo 2/fisiopatologia
Modelos Animais de Doenças
Progressão da Doença
Polipeptídeo Amiloide das Ilhotas Pancreáticas/genética
Polipeptídeo Amiloide das Ilhotas Pancreáticas/metabolismo
Luz
Masculino
Proteínas Circadianas Period/metabolismo
Ratos
Ratos Sprague-Dawley
Ratos Transgênicos
Núcleo Supraquiasmático/metabolismo
Núcleo Supraquiasmático/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Islet Amyloid Polypeptide); 0 (Period Circadian Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00406.2016


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[PMID]:29293553
[Au] Autor:Persons AL; Bradaric BD; Dodiya HB; Ohene-Nyako M; Forsyth CB; Keshavarzian A; Shaikh M; Napier TC
[Ad] Endereço:Department of Psychiatry, Rush University Medical Center, Chicago, IL, United States of America.
[Ti] Título:Colon dysregulation in methamphetamine self-administering HIV-1 transgenic rats.
[So] Source:PLoS One;13(1):e0190078, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The integrity and function of the gut is impaired in HIV-infected individuals, and gut pathogenesis may play a role in several HIV-associated disorders. Methamphetamine is a popular illicit drug abused by HIV-infected individuals. However, the effect of methamphetamine on the gut and its potential to exacerbate HIV-associated gut pathology is not known. To shed light on this scenario, we evaluated colon barrier pathology in a rat model of the human comorbid condition. Intestinal barrier integrity and permeability were assessed in drug-naïve Fischer 344 HIV-1 transgenic (Tg) and non-Tg rats, and in Tg and non-Tg rats instrumented with jugular cannulae trained to self-administer methamphetamine or serving as saline-yoked controls. Intestinal permeability was determined by measuring the urine content of orally gavaged sugars. Intestinal barrier integrity was evaluated by immunoblotting or immunofluorescence of colon claudin-1 and zonula occludens-1 (ZO-1), two major tight junction proteins that regulate gut epithelial paracellular permeability. Both non-Tg and Tg rats self-administered moderate amounts of methamphetamine. These amounts were sufficient to increase colon permeability, reduce protein level of claudin-1, and reduce claudin-1 and ZO-1 immunofluorescence in Tg rats relative to non-Tg rats. Methamphetamine decreased tight junction immunofluorescence in non-Tg rats, with a similar, but non-significant trend observed in Tg rats. However, the effect of methamphetamine on tight junction proteins was subthreshold to gut leakiness. These findings reveal that both HIV-1 proteins and methamphetamine alter colon barrier integrity, and indicate that the gut may be a pathogenic site for these insults.
[Mh] Termos MeSH primário: Colo/fisiopatologia
Infecções por HIV/fisiopatologia
HIV-1/genética
Metanfetamina/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Genótipo
Infecções por HIV/complicações
Mucosa Intestinal/fisiopatologia
Masculino
Ratos
Ratos Endogâmicos F344
Ratos Transgênicos
Autoadministração
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
44RAL3456C (Methamphetamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190078


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[PMID]:29267341
[Au] Autor:Abe K; Yawo H
[Ad] Endereço:Department of Development Biology and Neuroscience, Tohoku University Graduate School of Life Science, Sendai, Japan.
[Ti] Título:Optogenetic conditioning of paradigm and pattern discrimination in the rat somatosensory system.
[So] Source:PLoS One;12(12):e0189439, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The rodent whisker-barrel cortical system is a model for studying somatosensory discrimination at high spatiotemporal precision. Here, we applied optogenetics to produce somatosensory inputs in the whisker area using one of transgenic rat lines, W-TChR2V4, which expresses channelrhodopsin-2 (ChR2) in the mechanoreceptive nerve endings around whisker follicles. An awake W-TChR2V4 rat was head-fixed and irradiated by blue LED light on the whisker area with a paradigm conditioned with a reward. The Go task was designed so the rat is allowed to receive a reward, when it licked the nozzle within 5 s after photostimulation. The No-go task was designed so as the rat has to withhold licking for at least 5 s to obtain a reward after photostimulation. The Go-task conditioning was established within 1 hr of training with a reduction in the reaction time and increase of the success rate. To investigate the relationship between the spatiotemporal pattern of sensory inputs and the behavioral output, we designed a multi-optical fiber system that irradiates the whisker area at 9 spots in a 3×3 matrix. Although the Go-task conditioning was established using synchronous irradiation of 9 spots, the success rate was decreased with an increase of the reaction time for the asynchronous irradiation. After conditioning to the Go task, the rat responded to the blue LED flash irradiated on the barrel cortex, where many neurons also express ChR2, or photostimulation of the contralateral whisker area with a similar reaction time and success rate. Synchronous activation of the peripheral mechanoreceptive nerves is suggested to drive a neural circuit in the somatosensory cortex that efficiently couples with the decision. Our optogenetic system would enable the precise evaluation of the psychophysical values, such as the reaction time and success rate, to gain some insight into the brain mechanisms underlying conditioned behaviors.
[Mh] Termos MeSH primário: Optogenética
Córtex Somatossensorial/fisiologia
Vibrissas/fisiologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Condicionamento Operante
Ratos
Ratos Transgênicos
Tempo de Reação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189439


  4 / 1541 MEDLINE  
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[PMID]:29176843
[Au] Autor:Javadi-Paydar M; Roscoe RF; Denton AR; Mactutus CF; Booze RM
[Ad] Endereço:Behavioral Neuroscience Laboratory, Department of Psychology, University of South Carolina, Columbia, South Carolina, United States of America.
[Ti] Título:HIV-1 and cocaine disrupt dopamine reuptake and medium spiny neurons in female rat striatum.
[So] Source:PLoS One;12(11):e0188404, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HIV-1 and addictive drugs, such as cocaine (COC), may act in combination to produce serious neurological complications. In the present experiments, striatal brain slices from HIV-1 transgenic (Tg) and F344 control female rats were studied. First, we examined dopamine (DA) reuptake in control, HIV-1, COC-treated (5µM) and HIV-1+COC-treated, striatal slices using fast scan cyclic voltammetry. COC-treated striatal slices from F344 control animals significantly increased DA reuptake time (T80), relative to untreated control slices. In contrast, in HIV-1 Tg striatal slices, DA reuptake time was extended by HIV-1, which was not further altered by COC treatment. Second, analysis of medium spiny neuronal populations from striatal brain slices found that controls treated with cocaine displayed increases in spine length, whereas cocaine treated HIV-1 slices displayed decreased spine length. Taken together, the current study provides evidence for dysfunction of the dopamine transporter (DAT) in mediating DA reuptake in HIV-1 Tg rats and limited responses to acute COC exposure. Collectively, dysfunction of the DAT reuptake and altered dendritic spine morphology of the MSNs, suggest a functional disruption of the dopamine system within the HIV-1 Tg rat.
[Mh] Termos MeSH primário: Cocaína/farmacologia
Corpo Estriado/citologia
Dopamina/metabolismo
HIV-1/fisiologia
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Espinhas Dendríticas/efeitos dos fármacos
Espinhas Dendríticas/metabolismo
Feminino
Neurônios/efeitos dos fármacos
Núcleo Accumbens/efeitos dos fármacos
Núcleo Accumbens/metabolismo
Ratos Endogâmicos F344
Ratos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
I5Y540LHVR (Cocaine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188404


  5 / 1541 MEDLINE  
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[PMID]:29032151
[Au] Autor:Mandal K; Sarkar RK; Sen Sharma S; Jain A; Majumdar SS
[Ad] Endereço:Cellular Endocrinology Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India. Electronic address: kamal_mandal@nii.ac.in.
[Ti] Título:Sertoli cell specific knockdown of RAR-related orphan receptor (ROR) alpha at puberty reduces sperm count in rats.
[So] Source:Gene;641:18-24, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Globally, there is an alarming decline in sperm count. Very often hormonal supplementation fails to restore normal sperm count. Sertoli cells (Sc) present within seminiferous tubules provide appropriate niche and factors required for the differentiation of germ cells (Gc) into mature sperm (spermatogenesis). Functionally compromised Sc may be one of the reasons for failure of hormones to facilitate normal spermatogenesis. Although role of secretory proteins and signaling molecules of Sc has been studied well, role of transcription factors regulating sperm count has not been addressed appropriately. Retinoic acid receptor-related orphan receptor (ROR)-alpha is one of such transcription factors reported in testis but its role in testicular function is not yet known. In a separate study, we found abundant ROR-alpha binding sites on promoter regions of several genes upregulated in pubertal rat Sc as compared to infant Sc. Immunostaining studies also revealed presence of ROR alpha in nucleus of pubertal Sc. We generated a transgenic knockdown rat model expressing shRNA targeted to ROR-alpha under Sc specific promoter, which is transcriptionally active only at and after puberty. ROR-alpha knockdown animals were found to have abnormal association of Sc and Gc, including Gc sloughing and restricted release of sperm. The knockdown animals displayed compromised spermatogenesis leading to significant reduction in sperm count. This is the first report describing the Sc specific role of ROR-alpha in maintaining quantitatively normal sperm output. Identification of various such molecules can generate avenues to limit or reverse an alarmingly declining sperm count witnessed globally in men.
[Mh] Termos MeSH primário: Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/biossíntese
Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/genética
Células de Sertoli/metabolismo
Contagem de Espermatozoides
Espermatogênese/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Infertilidade Masculina/genética
Tamanho da Ninhada de Vivíparos/genética
Masculino
Interferência de RNA
RNA Interferente Pequeno/genética
Ratos
Ratos Transgênicos
Ratos Wistar
Espermatogênese/genética
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 1, Group F, Member 1); 0 (RNA, Small Interfering)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


  6 / 1541 MEDLINE  
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[PMID]:29040321
[Au] Autor:Goldman SM; Corona BT
[Ad] Endereço:United States Army Institute of Surgical Research, Fort Sam Houston, TX, United States of America.
[Ti] Título:Co-delivery of micronized urinary bladder matrix damps regenerative capacity of minced muscle grafts in the treatment of volumetric muscle loss injuries.
[So] Source:PLoS One;12(10):e0186593, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Minced muscle grafts (MG) promote de novo muscle fiber regeneration and neuromuscular strength recovery in small and large animal models of volumetric muscle loss. The most noteworthy limitation of this approach is its reliance on a finite supply of donor tissue. To address this shortcoming, this study sought to evaluate micronized acellular urinary bladder matrix (UBM) as a scaffolding to promote in vivo expansion of this MG therapy in a rat model. Rats received volumetric muscle loss injuries to the tibialis anterior muscle of their left hind limb which were either left untreated or repaired with minced muscle graft at dosages of 50% and 100% of the defect mass, urinary bladder matrix in isolation, or a with an expansion product consisting of a combination of the two putative therapies in which the minced graft is delivered at a dosage of 50% of the defect mass. Rats survived to 2 and 8 weeks post injury before functional (in vivo neuromuscular strength), histological, morphological, and biochemical analyses were performed. Rats treated with the expansion product exhibited improved neuromuscular function relative to untreated VML after an 8 week time period following injury. This improvement in functional capacity, however, was accompanied with a concomitant reduction in graft mediated regeneration, as evidenced cell lineage tracing enable by a transgenic GFP expressing donor, and a mixed histological outcome indicating coincident fibrous matrix deposition with interspersed islands of nascent muscle fibers. Furthermore, quantitative immunofluorescence and transcriptional analysis following the 2 week time point suggests an exacerbated immune response to the UBM as a possible nidus for the observed suboptimal regenerative outcome. Moving forward, efforts related to the development of a MG expansion product should carefully consider the effects of the host immune response to candidate biomaterials in order to avoid undesirable dysregulation of pro-regenerative cross talk between the immune system and myogenic processes.
[Mh] Termos MeSH primário: Músculo Esquelético/transplante
Regeneração/fisiologia
Tecidos Suporte
[Mh] Termos MeSH secundário: Animais
Matriz Extracelular/metabolismo
Masculino
Músculo Esquelético/lesões
Ratos
Ratos Endogâmicos Lew
Ratos Transgênicos
Recuperação de Função Fisiológica/fisiologia
Engenharia Tecidual
Transplante Homólogo/métodos
Bexiga Urinária/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186593


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[PMID]:28957681
[Au] Autor:Clements MP; Byrne E; Camarillo Guerrero LF; Cattin AL; Zakka L; Ashraf A; Burden JJ; Khadayate S; Lloyd AC; Marguerat S; Parrinello S
[Ad] Endereço:Cell Interactions and Cancer Group, MRC London Institute of Medical Sciences, Du Cane Road, London W12 0NN, United Kingdom; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, United Kingdom.
[Ti] Título:The Wound Microenvironment Reprograms Schwann Cells to Invasive Mesenchymal-like Cells to Drive Peripheral Nerve Regeneration.
[So] Source:Neuron;96(1):98-114.e7, 2017 Sep 27.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Schwann cell dedifferentiation from a myelinating to a progenitor-like cell underlies the remarkable ability of peripheral nerves to regenerate following injury. However, the molecular identity of the differentiated and dedifferentiated states in vivo has been elusive. Here, we profiled Schwann cells acutely purified from intact nerves and from the wound and distal regions of severed nerves. Our analysis reveals novel facets of the dedifferentiation response, including acquisition of mesenchymal traits and a Myc module. Furthermore, wound and distal dedifferentiated Schwann cells constitute different populations, with wound cells displaying increased mesenchymal character induced by localized TGFß signaling. TGFß promotes invasion and crosstalks with Eph signaling via N-cadherin to drive collective migration of the Schwann cells across the wound. Consistently, Tgfbr2 deletion in Schwann cells resulted in misdirected and delayed reinnervation. Thus, the wound microenvironment is a key determinant of Schwann cell identity, and it promotes nerve repair through integration of multiple concerted signals. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Diferenciação Celular
Microambiente Celular/fisiologia
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/fisiologia
Regeneração Nervosa/fisiologia
Traumatismos dos Nervos Periféricos/fisiopatologia
Células de Schwann/citologia
Células de Schwann/fisiologia
[Mh] Termos MeSH secundário: Animais
Caderinas/fisiologia
Movimento Celular/fisiologia
Células Cultivadas
Feminino
Masculino
Camundongos
Camundongos Transgênicos
Traumatismos dos Nervos Periféricos/patologia
Cultura Primária de Células
Ratos
Ratos Transgênicos
Receptores da Família Eph/fisiologia
Nervo Isquiático/lesões
Nervo Isquiático/fisiologia
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Transforming Growth Factor beta); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE


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[PMID]:28817668
[Au] Autor:Hassan N; McCarville K; Morinaga K; Mengatto CM; Langfelder P; Hokugo A; Tahara Y; Colwell CS; Nishimura I
[Ad] Endereço:Weintraub Center for Reconstructive Biotechnology, UCLA School of Dentistry, Los Angeles, California, United States of America.
[Ti] Título:Titanium biomaterials with complex surfaces induced aberrant peripheral circadian rhythms in bone marrow mesenchymal stromal cells.
[So] Source:PLoS One;12(8):e0183359, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Circadian rhythms maintain a high level of homeostasis through internal feed-forward and -backward regulation by core molecules. In this study, we report the highly unusual peripheral circadian rhythm of bone marrow mesenchymal stromal cells (BMSCs) induced by titanium-based biomaterials with complex surface modifications (Ti biomaterial) commonly used for dental and orthopedic implants. When cultured on Ti biomaterials, human BMSCs suppressed circadian PER1 expression patterns, while NPAS2 was uniquely upregulated. The Ti biomaterials, which reduced Per1 expression and upregulated Npas2, were further examined with BMSCs harvested from Per1::luc transgenic rats. Next, we addressed the regulatory relationship between Per1 and Npas2 using BMSCs from Npas2 knockout mice. The Npas2 knockout mutation did not rescue the Ti biomaterial-induced Per1 suppression and did not affect Per2, Per3, Bmal1 and Clock expression, suggesting that the Ti biomaterial-induced Npas2 overexpression was likely an independent phenomenon. Previously, vitamin D deficiency was reported to interfere with Ti biomaterial osseointegration. The present study demonstrated that vitamin D supplementation significantly increased Per1::luc expression in BMSCs, though the presence of Ti biomaterials only moderately affected the suppressed Per1::luc expression. Available in vivo microarray data from femurs exposed to Ti biomaterials in vitamin D-deficient rats were evaluated by weighted gene co-expression network analysis. A large co-expression network containing Npas2, Bmal1, and Vdr was observed to form with the Ti biomaterials, which was disintegrated by vitamin D deficiency. Thus, the aberrant BMSC peripheral circadian rhythm may be essential for the integration of Ti biomaterials into bone.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Células da Medula Óssea/citologia
Ritmo Circadiano
Células Mesenquimais Estromais/citologia
Titânio/química
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Seres Humanos
Ratos
Ratos Transgênicos
Ratos Wistar
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); D1JT611TNE (Titanium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183359


  9 / 1541 MEDLINE  
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[PMID]:28808062
[Au] Autor:Whitfield J; Paglialunga S; Smith BK; Miotto PM; Simnett G; Robson HL; Jain SS; Herbst EAF; Desjardins EM; Dyck DJ; Spriet LL; Steinberg GR; Holloway GP
[Ad] Endereço:From the Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada and.
[Ti] Título:Ablating the protein TBC1D1 impairs contraction-induced sarcolemmal glucose transporter 4 redistribution but not insulin-mediated responses in rats.
[So] Source:J Biol Chem;292(40):16653-16664, 2017 Oct 06.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TBC1 domain family member 1 (TBC1D1), a Rab GTPase-activating protein and paralogue of Akt substrate of 160 kDa (AS160), has been implicated in both insulin- and 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase-mediated glucose transporter type 4 (GLUT4) translocation. However, the role of TBC1D1 in contracting muscle remains ambiguous. We therefore explored the metabolic consequence of ablating TBC1D1 in both resting and contracting skeletal muscles, utilizing a rat TBC1D1 KO model. Although insulin administration rapidly increased ( < 0.05) plasma membrane GLUT4 content in both red and white gastrocnemius muscles, the TBC1D1 ablation did not alter this response nor did it affect whole-body insulin tolerance, suggesting that TBC1D1 is not required for insulin-induced GLUT4 trafficking events. Consistent with findings in other models of altered TBC1D1 protein levels, whole-animal and skeletal muscle fat oxidation was increased in the TBC1D1 KO rats. Although there was no change in mitochondrial content in the KO rats, maximal ADP-stimulated respiration was higher in permeabilized muscle fibers, which may contribute to the increased reliance on fatty acids in resting KO animals. Despite this increase in mitochondrial oxidative capacity, run time to exhaustion at various intensities was impaired in the KO rats. Moreover, contraction-induced increases in sarcolemmal GLUT4 content and glucose uptake were lower in the white gastrocnemius of the KO animals. Altogether, our results highlight a critical role for TBC1D1 in exercise tolerance and contraction-mediated translocation of GLUT4 to the plasma membrane in skeletal muscle.
[Mh] Termos MeSH primário: Tolerância ao Exercício/fisiologia
Transportador de Glucose Tipo 4/metabolismo
Contração Muscular/fisiologia
Músculo Esquelético/metabolismo
Proteínas/metabolismo
Sarcolema/metabolismo
[Mh] Termos MeSH secundário: Animais
Transportador de Glucose Tipo 4/genética
Insulina/genética
Insulina/metabolismo
Oxirredução
Consumo de Oxigênio/fisiologia
Transporte Proteico/fisiologia
Proteínas/genética
Ratos
Ratos Sprague-Dawley
Ratos Transgênicos
Sarcolema/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 4); 0 (Insulin); 0 (Proteins); 0 (Slc2a4 protein, rat); 0 (TBC1D1 protein, rat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.806786


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[PMID]:28779019
[Au] Autor:Whitaker LR; Warren BL; Venniro M; Harte TC; McPherson KB; Beidel J; Bossert JM; Shaham Y; Bonci A; Hope BT
[Ad] Endereço:Behavioral Neuroscience Research Branch and leslie.ramsey@nih.gov.
[Ti] Título:Bidirectional Modulation of Intrinsic Excitability in Rat Prelimbic Cortex Neuronal Ensembles and Non-Ensembles after Operant Learning.
[So] Source:J Neurosci;37(36):8845-8856, 2017 Sep 06.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Learned associations between environmental stimuli and rewards drive goal-directed learning and motivated behavior. These memories are thought to be encoded by alterations within specific patterns of sparsely distributed neurons called neuronal ensembles that are activated selectively by reward-predictive stimuli. Here, we use the Fos promoter to identify strongly activated neuronal ensembles in rat prelimbic cortex (PLC) and assess altered intrinsic excitability after 10 d of operant food self-administration training (1 h/d). First, we used the Daun02 inactivation procedure in male FosLacZ-transgenic rats to ablate selectively Fos-expressing PLC neurons that were active during operant food self-administration. Selective ablation of these neurons decreased food seeking. We then used male FosGFP-transgenic rats to assess selective alterations of intrinsic excitability in Fos-expressing neuronal ensembles (FosGFP ) that were activated during food self-administration and compared these with alterations in less activated non-ensemble neurons (FosGFP ). Using whole-cell recordings of layer V pyramidal neurons in an brain slice preparation, we found that operant self-administration increased excitability of FosGFP neurons and decreased excitability of FosGFP neurons. Increased excitability of FosGFP neurons was driven by increased steady-state input resistance. Decreased excitability of FosGFP neurons was driven by increased contribution of small-conductance calcium-activated potassium (SK) channels. Injections of the specific SK channel antagonist apamin into PLC increased Fos expression but had no effect on food seeking. Overall, operant learning increased intrinsic excitability of PLC Fos-expressing neuronal ensembles that play a role in food seeking but decreased intrinsic excitability of Fos non-ensembles. Prefrontal cortex activity plays a critical role in operant learning, but the underlying cellular mechanisms are unknown. Using the chemogenetic Daun02 inactivation procedure, we found that a small number of strongly activated Fos-expressing neuronal ensembles in rat PLC play an important role in learned operant food seeking. Using GFP expression to identify Fos-expressing layer V pyramidal neurons in prelimbic cortex (PLC) of FosGFP-transgenic rats, we found that operant food self-administration led to increased intrinsic excitability in the behaviorally relevant Fos-expressing neuronal ensembles, but decreased intrinsic excitability in Fos neurons using distinct cellular mechanisms.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Aprendizagem por Associação/fisiologia
Condicionamento Operante/fisiologia
Rede Nervosa/fisiologia
Plasticidade Neuronal/fisiologia
Córtex Pré-Frontal/fisiologia
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Long-Evans
Ratos Sprague-Dawley
Ratos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3761-16.2017



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