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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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