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[PMID]:29371650
[Au] Autor:Sheikhbahaei S; Turovsky EA; Hosford PS; Hadjihambi A; Theparambil SM; Liu B; Marina N; Teschemacher AG; Kasparov S; Smith JC; Gourine AV
[Ad] Endereço:Centre for Cardiovascular and Metabolic Neuroscience, Department of Neuroscience, Physiology and Pharmacology, University College London, London, WC1E 6BT, UK.
[Ti] Título:Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.
[So] Source:Nat Commun;9(1):370, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Astrocytes are implicated in modulation of neuronal excitability and synaptic function, but it remains unknown if these glial cells can directly control activities of motor circuits to influence complex behaviors in vivo. This study focused on the vital respiratory rhythm-generating circuits of the preBötzinger complex (preBötC) and determined how compromised function of local astrocytes affects breathing in conscious experimental animals (rats). Vesicular release mechanisms in astrocytes were disrupted by virally driven expression of either the dominant-negative SNARE protein or light chain of tetanus toxin. We show that blockade of vesicular release in preBötC astrocytes reduces the resting breathing rate and frequency of periodic sighs, decreases rhythm variability, impairs respiratory responses to hypoxia and hypercapnia, and dramatically reduces the exercise capacity. These findings indicate that astrocytes modulate the activity of CNS circuits generating the respiratory rhythm, critically contribute to adaptive respiratory responses in conditions of increased metabolic demand and determine the exercise capacity.
[Mh] Termos MeSH primário: Astrócitos/fisiologia
Tronco Encefálico/fisiologia
Periodicidade
Condicionamento Físico Animal/fisiologia
Respiração
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Adenoviridae/genética
Adenoviridae/metabolismo
Animais
Animais Recém-Nascidos
Astrócitos/citologia
Tronco Encefálico/citologia
Cálcio/metabolismo
Feminino
Regulação da Expressão Gênica
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Hipercapnia/metabolismo
Hipercapnia/fisiopatologia
Hipóxia/metabolismo
Hipóxia/fisiopatologia
Masculino
Bulbo/citologia
Bulbo/fisiologia
Cultura Primária de Células
Ratos
Ratos Sprague-Dawley
Proteínas SNARE/antagonistas & inibidores
Proteínas SNARE/genética
Proteínas SNARE/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SNARE Proteins); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02723-6


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[PMID]:28461605
[Au] Autor:Gao L; Zimmerman MC; Biswal S; Zucker IH
[Ad] Endereço:From the Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Nebraska Medical Center, Omaha (L.G., M.C.Z., I.H.Z.); and Department of Environmental Health and Engineering, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD (S.B.).
[Ti] Título:Selective Gene Deletion in the Rostral Ventrolateral Medulla Evokes Hypertension and Sympathoexcitation in Mice.
[So] Source:Hypertension;69(6):1198-1206, 2017 06.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master transcriptional regulator of redox homeostasis that impacts antioxidant gene expression. Central oxidative stress and reduced antioxidant enzyme expression in the rostral ventrolateral medulla (RVLM) contributed to sympathoexcitation in chronic heart failure. In the current study, we hypothesized that deletion of Nrf2 in the RVLM would increase sympathetic drive and blood pressure. Experiments were performed in Nrf2-floxed mice treated with microinjection of lentiviral-Cre-GFP or lentiviral-GFP into the RVLM. Two weeks after viral administration, Nrf2 message, protein, oxidative stress, cardiovascular function, and sympathetic outflow were evaluated. We found that (1) Nrf2 mRNA and protein in the RVLM were significantly lower in Cre mice compared with control GFP mice. Nrf2-targeted antioxidant enzymes were downregulated, whereas reactive oxygen species were elevated. (2) Blood pressure measurements indicated that Cre mice displayed a significant increase in blood pressure (mean arterial pressure, 123.7±3.8 versus 100.2±2.2 mm Hg; <0.05, n=6), elevated urinary norepinephrine (NE) concentration (456.4±16.9 versus 356.5±19.9 ng/mL; <0.05, n=6), and decreased spontaneous baroreflex gain (up sequences, 1.66±0.17 versus 3.61±0.22 ms/mm Hg; <0.05, n=6; down sequences, 1.89±0.12 versus 2.98±0.19 ms/mm Hg; <0.05, n=6). (3) Cre mice displayed elevated baseline renal sympathetic nerve activity and impaired inducible baroreflex function. These data suggest that gene deletion in the RVLM elevates blood pressure, increases sympathetic outflow, and impairs baroreflex function potentially by impaired antioxidant enzyme expression.
[Mh] Termos MeSH primário: Deleção de Genes
Hipertensão/genética
Bulbo/metabolismo
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/genética
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Barorreflexo/fisiologia
Determinação da Pressão Arterial/métodos
Modelos Animais de Doenças
Hipertensão Essencial
Feminino
Frequência Cardíaca/fisiologia
Homeostase
Hipertensão/fisiopatologia
Masculino
Camundongos
Oxirredução
RNA Mensageiro/análise
Distribuição Aleatória
Reação em Cadeia da Polimerase em Tempo Real/métodos
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antioxidants); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (RNA, Messenger)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09123


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[PMID]:29032150
[Au] Autor:Sundararajan T; Manzardo AM; Butler MG
[Ad] Endereço:Department of Psychiatry and Behavioral Sciences, University of Kansas Medical Center, Kansas City, KS, United States.
[Ti] Título:Functional analysis of schizophrenia genes using GeneAnalytics program and integrated databases.
[So] Source:Gene;641:25-34, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Schizophrenia (SCZ) is a chronic debilitating neuropsychiatric disorder with multiple risk factors involving numerous complex genetic influences. We examined and updated a master list of clinically relevant and susceptibility genes associated with SCZ reported in the literature and genomic databases dedicated to gene discovery for characterization of SCZ genes. We used the commercially available GeneAnalytics computer-based gene analysis program and integrated genomic databases to create a molecular profile of the updated list of 608 SCZ genes to model their impact in select categories (tissues and cells, diseases, pathways, biological processes, molecular functions, phenotypes and compounds) using specialized GeneAnalytics algorithms. Genes for schizophrenia were predominantly expressed in the cerebellum, cerebral cortex, medulla oblongata, thalamus and hypothalamus. Psychiatric/behavioral disorders incorporating SCZ genes included ADHD, bipolar disorder, autism spectrum disorder and alcohol dependence as well as cancer, Alzheimer's and Parkinson's disease, sleep disturbances and inflammation. Function based analysis of major biological pathways and mechanisms associated with SCZ genes identified glutaminergic receptors (e.g., GRIA1, GRIN2, GRIK4, GRM5), serotonergic receptors (e.g., HTR2A, HTR2C), GABAergic receptors (e.g., GABRA1, GABRB2), dopaminergic receptors (e.g., DRD1, DRD2), calcium-related channels (e.g., CACNA1H, CACNA1B), solute transporters (e.g., SLC1A1, SLC6A2) and for neurodevelopment (e.g., ADCY1, MEF2C, NOTCH2, SHANK3). Biological mechanisms involving synaptic transmission, regulation of membrane potential and transmembrane ion transport were identified as leading molecular functions associated with SCZ genes. Our approach to interrogate SCZ genes and their interactions at various levels has increased our knowledge and insight into the disease process possibly opening new avenues for therapeutic intervention.
[Mh] Termos MeSH primário: Estudo de Associação Genômica Ampla
Transporte de Íons/genética
Potenciais da Membrana/genética
Esquizofrenia/genética
Transmissão Sináptica/genética
[Mh] Termos MeSH secundário: Sistemas de Transporte de Aminoácidos/genética
Canais de Cálcio/genética
Cerebelo/citologia
Córtex Cerebral/citologia
Bases de Dados Genéticas
Seres Humanos
Hipotálamo/citologia
Bulbo/citologia
Receptores Dopaminérgicos/genética
Receptores de GABA-A/genética
Receptores Ionotrópicos de Glutamato/genética
Receptores de Serotonina/genética
Tálamo/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems); 0 (Calcium Channels); 0 (Receptors, Dopamine); 0 (Receptors, GABA-A); 0 (Receptors, Ionotropic Glutamate); 0 (Receptors, Serotonin)
[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


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[PMID]:28931039
[Au] Autor:Bright FM; Vink R; Byard RW; Duncan JR; Krous HF; Paterson DS
[Ad] Endereço:Discipline of Anatomy and Pathology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
[Ti] Título:Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex.
[So] Source:PLoS One;12(9):e0184958, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sudden infant death syndrome (SIDS) involves failure of arousal to potentially life threatening events, including hypoxia, during sleep. While neuronal dysfunction and abnormalities in neurotransmitter systems within the medulla oblongata have been implicated, the specific pathways associated with autonomic and cardiorespiratory failure are unknown. The neuropeptide substance P (SP) and its tachykinin neurokinin-1 receptor (NK1R) have been shown to play an integral role in the modulation of homeostatic function in the medulla, including regulation of respiratory rhythm generation, integration of cardiovascular control, and modulation of the baroreceptor reflex and mediation of the chemoreceptor reflex in response to hypoxia. Abnormalities in SP neurotransmission may therefore result in autonomic dysfunction during sleep and contribute to SIDS deaths. [125I] Bolton Hunter SP autoradiography was used to map the distribution and density of the SP, NK1R to 13 specific nuclei intimately related to cardiorespiratory function and autonomic control in the human infant medulla of 55 SIDS and 21 control (non-SIDS) infants. Compared to controls, SIDS cases exhibited a differential, abnormal developmental profile of the SP/NK1R system in the medulla. Furthermore the study revealed significantly decreased NK1R binding within key medullary nuclei in SIDS cases, principally in the nucleus tractus solitarii (NTS) and all three subdivisions of the inferior portion of the olivo-cerebellar complex; the principal inferior olivary complex (PIO), medial accessory olive (MAO) and dorsal accessory olive (DAO). Altered NK1R binding was significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants. Abnormal NK1R binding in these medullary nuclei may contribute to the defective interaction of critical medullary mechanisms with cerebellar sites, resulting in an inability of a SIDS infant to illicit appropriate respiratory and motor responses to life threatening challenges during sleep. These observations support the concept that abnormalities in a multi-neurotransmitter network within key nuclei of the medullary homeostatic system may underlie the pathogenesis of a subset of SIDS cases.
[Mh] Termos MeSH primário: Tronco Encefálico/patologia
Recém-Nascido Prematuro/metabolismo
Bulbo/patologia
Núcleo Olivar/patologia
Receptores da Neurocinina-1/metabolismo
Substância P/metabolismo
Morte Súbita do Lactente/patologia
[Mh] Termos MeSH secundário: Tronco Encefálico/metabolismo
Estudos de Coortes
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Bulbo/metabolismo
Núcleo Olivar/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Neurokinin-1); 33507-63-0 (Substance P)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184958


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[PMID]:28922849
[Au] Autor:Bright FM; Byard RW; Vink R; Paterson DS
[Ad] Endereço:Faculty of Health and Medical Science, School of Medicine, University of Adelaide, Adelaide, South Australia, Australia; Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts; Sansom Institute for Health Research, University of South Australia, Adelaid
[Ti] Título:Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome.
[So] Source:J Neuropathol Exp Neurol;76(10):864-873, 2017 Oct 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Serotonin (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to key autonomic and respiratory nuclei in the brainstem and spinal cord regulating critical homeostatic functions. Multiple abnormalities in markers of 5-HT function in the medulla in sudden infant death syndrome (SIDS) have been reported, informing the hypothesis that at least a subset of SIDS cases is caused by deficits in 5-HT function resulting in impaired homeostatic responses to potentially life-threatening events during sleep. To investigate medullary 5-HT defects in SIDS further, we undertook qualitative analysis immunohistochemical assessment of 5-HT neuron expression within the medulla of SIDS infants (n41) and nonSIDS controls (n = 28) in an independent cohort from Forensic Science South Australia. Compared with controls SIDS cases had significantly higher 5-HT neuron numbers and density in addition to significantly altered 5-HT neuron morphology. Thus, for the first time, we replicated and corroborated previous observations of a significant abnormality in medullary 5-HT neuron expression in SIDS in a separate independent SIDS cohort. This study further supports the hypothesis that medullary 5-HT defects contribute to the pathogenesis of a subset of SIDS victims and provides additional evidence of a more complex abnormality in 5-HT neuron dysfunction specifically within the different caudal and rostral medullary 5-HT domains.
[Mh] Termos MeSH primário: Bulbo/patologia
Neurônios/patologia
Serotonina/metabolismo
Morte Súbita do Lactente/epidemiologia
Morte Súbita do Lactente/patologia
[Mh] Termos MeSH secundário: Austrália/epidemiologia
Contagem de Células
Estudos de Coortes
Bases de Dados Factuais/estatística & dados numéricos
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Neurônios/metabolismo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
333DO1RDJY (Serotonin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx071


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[PMID]:28816948
[Au] Autor:Yanagiha K; Ishii K; Ueno T; Marushima A; Tamaoka A
[Ad] Endereço:aDepartment of Neurology bDepartment of Rehabilitation Medicine, University of Tsukuba Hospital cDepartment of Emergency and Critical Care Medicine, Division of Clinical Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
[Ti] Título:Medial medullary infarction caused by antineutrophil cytoplasmic antibody-related vasculitis: Case report and review of the literature.
[So] Source:Medicine (Baltimore);96(33):e7722, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Medial medullary infarction accounts for less than 1% of brain infarctions, and medial medullary infarctions is very rarely caused by antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. PATIENT CONCERNS: We report the case of a 76-year-old man at low risk of arteriosclerosis who presented with disorders on the left side including gaze-evoked nystagmus, paralysis of the extremities, pyramidal signs, sensory disturbance, and dysesthesia. Brain magnetic resonance imaging also showed right medial medullary infarction. DIAGNOSES: Medial medullary infarction caused by ANCA-related vasculitis was diagnosed based on mild renal dysfunction and high levels of blood leukocytes, C-reactive protein (CRP), and myeloperoxidase (MPO)-ANCA. INTERVENTIONS AND OUTCOMES: He underwent two 3-day courses of steroid pulse therapy involving daily 1000 mg doses of methylpredonine. He then received 30 mg/day (0.5 mg/kg/day) of prednisolone (PSL) without other immunosuppressants. Levels of MPO-ANCA and the inflammatory marker CRP decreased rapidly a month after admission. Once MPO-ANCA became undetectable, the PSL dose was carefully reduced to 10 mg/day. To treat his paralysis, we provided rehabilitation with a Hybrid Assistive Limb five times starting at a month post-onset. His Barthel index score rose from 45 to 70 points. LESSONS: Medullary infarction is mostly caused by arteriosclerosis and vertebral arterial dissection. When systemic inflammatory findings are obtained, ANCA-associated vasculitis should be considered a potential cause, and steroid pulse therapy should be promptly administered.
[Mh] Termos MeSH primário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/complicações
Infarto Encefálico/diagnóstico
Infarto Encefálico/etiologia
[Mh] Termos MeSH secundário: Corticosteroides/uso terapêutico
Idoso
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/tratamento farmacológico
Infarto Encefálico/diagnóstico por imagem
Proteína C-Reativa/análise
Seres Humanos
Imunossupressores/uso terapêutico
Contagem de Leucócitos
Imagem por Ressonância Magnética
Masculino
Bulbo/patologia
Peroxidase/sangue
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Immunosuppressive Agents); 9007-41-4 (C-Reactive Protein); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007722


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[PMID]:28700706
[Au] Autor:Freundt-Revilla J; Kegler K; Baumgärtner W; Tipold A
[Ad] Endereço:Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover Foundation, Hannover, Germany.
[Ti] Título:Spatial distribution of cannabinoid receptor type 1 (CB1) in normal canine central and peripheral nervous system.
[So] Source:PLoS One;12(7):e0181064, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The endocannabinoid system is a regulatory pathway consisting of two main types of cannabinoid receptors (CB1 and CB2) and their endogenous ligands, the endocannabinoids. The CB1 receptor is highly expressed in the central and peripheral nervous systems (PNS) in mammalians and is involved in neuromodulatory functions. Since endocannabinoids were shown to be elevated in cerebrospinal fluid of epileptic dogs, knowledge about the species specific CB receptor expression in the nervous system is required. Therefore, we assessed the spatial distribution of CB1 receptors in the normal canine CNS and PNS. Immunohistochemistry of several regions of the brain, spinal cord and peripheral nerves from a healthy four-week-old puppy, three six-month-old dogs, and one ten-year-old dog revealed strong dot-like immunoreactivity in the neuropil of the cerebral cortex, Cornu Ammonis (CA) and dentate gyrus of the hippocampus, midbrain, cerebellum, medulla oblongata and grey matter of the spinal cord. Dense CB1 expression was found in fibres of the globus pallidus and substantia nigra surrounding immunonegative neurons. Astrocytes were constantly positive in all examined regions. CB1 labelled neurons and satellite cells of the dorsal root ganglia, and myelinating Schwann cells in the PNS. These results demonstrate for the first time the spatial distribution of CB1 receptors in the healthy canine CNS and PNS. These results can be used as a basis for further studies aiming to elucidate the physiological consequences of this particular anatomical and cellular distribution.
[Mh] Termos MeSH primário: Sistema Nervoso Periférico/metabolismo
Receptor CB1 de Canabinoide/metabolismo
[Mh] Termos MeSH secundário: Animais
Moduladores de Receptores de Canabinoides/metabolismo
Cerebelo/metabolismo
Córtex Cerebral/metabolismo
Giro Denteado/metabolismo
Cães
Feminino
Gânglios Espinais/metabolismo
Hipocampo/metabolismo
Imuno-Histoquímica
Masculino
Bulbo/metabolismo
Mesencéfalo/metabolismo
Bulbo Olfatório/metabolismo
Nervos Periféricos/metabolismo
Receptor CB1 de Canabinoide/genética
Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cannabinoid Receptor Modulators); 0 (Receptor, Cannabinoid, CB1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181064


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[PMID]:28676575
[Au] Autor:Skyberg R; Sun C; Hill DL
[Ad] Endereço:Department of Psychology, University of Virginia, Charlottesville, Virginia 22904-4400.
[Ti] Título:Maintenance of Mouse Gustatory Terminal Field Organization Is Disrupted following Selective Removal of Peripheral Sodium Salt Taste Activity at Adulthood.
[So] Source:J Neurosci;37(32):7619-7630, 2017 Aug 09.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neural activity plays a critical role in the development of central circuits in sensory systems. However, the maintenance of these circuits at adulthood is usually not dependent on sensory-elicited neural activity. Recent work in the mouse gustatory system showed that selectively deleting the primary transduction channel for sodium taste, the epithelial sodium channel (ENaC), throughout development dramatically impacted the organization of the central terminal fields of three nerves that carry taste information to the nucleus of the solitary tract. More specifically, deleting ENaCs during development prevented the normal maturation of the fields. The present study was designed to extend these findings by testing the hypothesis that the loss of sodium taste activity impacts the maintenance of the normal adult terminal field organization in male and female mice. To do this, we used an inducible Cre-dependent genetic recombination strategy to delete ENaC function after terminal field maturation occurred. We found that removal of sodium taste neural activity at adulthood resulted in significant reorganization of mature gustatory afferent terminal fields in the nucleus of the solitary tract. Specifically, the chorda tympani and greater superficial petrosal nerve terminal fields were 1.4× and 1.6× larger than age-matched controls, respectively. By contrast, the glossopharyngeal nerve, which is not highly sensitive to sodium taste stimulation, did not undergo terminal field reorganization. These surprising results suggest that gustatory nerve terminal fields remain plastic well into adulthood, which likely impacts central coding of taste information and taste-related behaviors with altered taste experience. Neural activity plays a major role in the development of sensory circuits in the mammalian brain. However, the importance of sensory-driven activity in maintaining these circuits at adulthood, especially in subcortical structures, appears to be much less. Here, we tested whether the loss of sodium taste activity in adult mice impacts the maintenance of how taste nerves project to the first central relay. We found that specific loss of sodium-elicited taste activity at adulthood produced dramatic and selective reorganization of terminal fields in the brainstem. This demonstrates, for the first time, that taste-elicited activity is necessary for the normal maintenance of central gustatory circuits at adulthood and highlights a level of plasticity not seen in other sensory system subcortical circuits.
[Mh] Termos MeSH primário: Bulbo/fisiologia
Sódio na Dieta/administração & dosagem
Papilas Gustativas/fisiologia
Percepção Gustatória/fisiologia
Paladar/fisiologia
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Feminino
Nervo Glossofaríngeo/efeitos dos fármacos
Nervo Glossofaríngeo/fisiologia
Nervo Hipoglosso/efeitos dos fármacos
Nervo Hipoglosso/fisiologia
Masculino
Bulbo/efeitos dos fármacos
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Terminações Pré-Sinápticas/efeitos dos fármacos
Terminações Pré-Sinápticas/fisiologia
Papilas Gustativas/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sodium, Dietary)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3838-16.2017


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[PMID]:28625488
[Au] Autor:Zhao Z; Wang L; Gao W; Hu F; Zhang J; Ren Y; Lin R; Feng Q; Cheng M; Ju D; Chi Q; Wang D; Song S; Luo M; Zhan C
[Ad] Endereço:National Institute of Biological Sciences, Beijing, 102206, China.
[Ti] Título:A Central Catecholaminergic Circuit Controls Blood Glucose Levels during Stress.
[So] Source:Neuron;95(1):138-152.e5, 2017 Jul 05.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stress-induced hyperglycemia is a fundamental adaptive response that mobilizes energy stores in response to threats. Here, our examination of the contributions of the central catecholaminergic (CA) neuronal system to this adaptive response revealed that CA neurons in the ventrolateral medulla (VLM) control stress-induced hyperglycemia. Ablation of VLM CA neurons abolished the hyperglycemic response to both physical and psychological stress, whereas chemogenetic activation of these neurons was sufficient to induce hyperglycemia. We further found that CA neurons in the rostral VLM, but not those in the caudal VLM, cause hyperglycemia via descending projections to the spinal cord. Monosynaptic tracing experiments showed that VLM CA neurons receive direct inputs from multiple stress-responsive brain areas. Optogenetic studies identified an excitatory PVN-VLM circuit that induces hyperglycemia. This study establishes the central role of VLM CA neurons in stress-induced hyperglycemia and substantially expands our understanding of the central mechanism that controls glucose metabolism.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Catecolaminas/metabolismo
Hiperglicemia/metabolismo
Bulbo/metabolismo
Núcleo Hipotalâmico Paraventricular/metabolismo
Estresse Fisiológico/fisiologia
Estresse Psicológico/metabolismo
[Mh] Termos MeSH secundário: Animais
Lipopolissacarídeos
Bulbo/fisiologia
Camundongos
Vias Neurais/fisiologia
Núcleo Hipotalâmico Paraventricular/fisiologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Catecholamines); 0 (Lipopolysaccharides); 0 (Proto-Oncogene Proteins c-fos)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


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[PMID]:28609288
[Au] Autor:Osacka J; Horvathova L; Majercikova Z; Kiss A
[Ad] Endereço:.
[Ti] Título:Eff ect of a single asenapine treatment on Fos expression in the brain catecholamine-synthesizing neurons: impact of a chronic mild stress preconditioning.
[So] Source:Endocr Regul;51(2):73-83, 2017 Apr 25.
[Is] ISSN:1210-0668
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Fos protein expression in catecholamine-synthesizing neurons of the substantia nigra (SN) pars compacta (SNC, A8), pars reticulata (SNR, A9), and pars lateralis (SNL), the ventral tegmental area (VTA, A10), the locus coeruleus (LC, A6) and subcoeruleus (sLC), the ventrolateral pons (PON-A5), the nucleus of the solitary tract (NTS-A2), the area postrema (AP), and the ventrolateral medulla (VLM-A1) was quantitatively evaluated aft er a single administration of asenapine (ASE) (designated for schizophrenia treatment) in male Wistar rats preconditioned with a chronic unpredictable variable mild stress (CMS) for 21 days. Th e aim of the present study was to reveal whether a single ASE treatment may 1) activate Fos expression in the brain areas selected; 2) activate tyrosine hydroxylase (TH)-synthesizing cells displaying Fos presence; and 3) be modulated by CMS preconditioning. METHODS: Control (CON), ASE, CMS, and CMS+ASE groups were used. CMS included restraint, social isolation, crowding, swimming, and cold. Th e ASE and CMS+ASE groups received a single dose of ASE (0.3 mg/kg, s.c.) and CON and CMS saline (300 µl/rat, s.c.). The animals were sacrificed 90 min aft er the treatments. Fos protein and TH-labeled immunoreactive perikarya were analyzed on double labeled histological sections and enumerated on captured pictures using combined light and fluorescence microscope illumination. RESULTS: Saline or CMS alone did not promote Fos expression in any of the structures investigated. ASE alone or in combination with CMS elicited Fos expression in two parts of the SN (SNC, SNR) and the VTA. Aside from some cells in the central gray tegmental nuclei adjacent to LC, where a small number of Fos profiles occurred, none or negligible Fos occurrence was detected in the other structures investigated including the LC and sLC, PON-A5, NTS-A2, AP, and VLM-A1. CMS preconditioning did not infl uence the level of Fos induction in the SN and VTA elicited by ASE administration. Similarly, the ratio between the amount of free Fos and Fos colocalized with TH was not aff ected by stress preconditioning in the SNC, SNR, and the VTA. CONCLUSIONS: Th e present study provides an anatomical/functional knowledge about the nature of the acute ASE treatment on the catecholamine-synthesizing neurons activity in certain brain structures and their missing interplay with the CMS preconditioning.
[Mh] Termos MeSH primário: Antipsicóticos/farmacologia
Encéfalo/efeitos dos fármacos
Condicionamento (Psicologia)
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Neurônios/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/efeitos dos fármacos
Estresse Psicológico/metabolismo
Tirosina 3-Mono-Oxigenase/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Área Postrema/citologia
Área Postrema/efeitos dos fármacos
Área Postrema/metabolismo
Encéfalo/citologia
Encéfalo/metabolismo
Catecolaminas/biossíntese
Imuno-Histoquímica
Locus Cerúleo/citologia
Locus Cerúleo/efeitos dos fármacos
Locus Cerúleo/metabolismo
Masculino
Bulbo/citologia
Bulbo/efeitos dos fármacos
Bulbo/metabolismo
Microscopia de Fluorescência
Neurônios/metabolismo
Parte Compacta da Substância Negra/citologia
Parte Compacta da Substância Negra/efeitos dos fármacos
Parte Compacta da Substância Negra/metabolismo
Parte Reticular da Substância Negra/citologia
Parte Reticular da Substância Negra/efeitos dos fármacos
Parte Reticular da Substância Negra/metabolismo
Ponte/citologia
Ponte/efeitos dos fármacos
Ponte/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Wistar
Núcleo Solitário/citologia
Núcleo Solitário/efeitos dos fármacos
Núcleo Solitário/metabolismo
Estresse Psicológico/psicologia
Tirosina 3-Mono-Oxigenase/metabolismo
Área Tegmentar Ventral/citologia
Área Tegmentar Ventral/efeitos dos fármacos
Área Tegmentar Ventral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Catecholamines); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Proto-Oncogene Proteins c-fos); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); JKZ19V908O (Asenapine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE



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