Biomedical Science
Mizoguchi Y, Monji A, Kato TA, Horikawa H, Seki Y, Kasai M, Kanba S, Yamada S.
Mini Rev Med Chem. 2011 Jun;11(7):575-81.
Microglia are intrinsic immune cells that release factors, including proinflammatory cytokines, nitric oxide (NO) and neurotrophins, following activation after disturbance in the brain. Elevation of intracellular Ca(2+) concentration ([Ca(2+)]i) is important for microglial functions, such as the release of cytokines and NO from activated microglia. There is increasing evidence suggesting that pathophysiology of neuropsychiatric disorders is related to the inflammatory responses mediated by microglia. Brain-derived neurotrophic factor (BDNF) is a neurotrophin well known for its roles in the activation of microglia as well as in pathophysiology and/or treatment of neuropsychiatric disorders.
Possible role of BDNF-induced microglial intracellular Ca(2+) elevation in the pathophysiology of neuropsychiatric disorders
Read more...Dominance, politics, and physiology: voters' testosterone changes on the night of the 2008 United States presidential election
Stanton SJ, Beehner JC, Saini EK, Kuhn CM, Labar KS.
Center for Cognitive Neuroscience, Duke University, Durham, North Carolina, United States of America.
PLoS One. 2009 Oct 21;4(10):e7543.
BACKGROUND: Political elections are dominance competitions. When men win a dominance competition, their testosterone levels rise or remain stable to resist a circadian decline; and when they lose, their testosterone levels fall. However, it is unknown whether this pattern of testosterone change extends beyond interpersonal competitions to the vicarious experience of winning or losing in the context of political elections. Women's testosterone responses to dominance competition outcomes are understudied, and to date, a clear pattern of testosterone changes in response to winning and losing dominance competitions has not emerged.
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Center for Cognitive Neuroscience, Duke University, Durham, North Carolina, United States of America.
PLoS One. 2009 Oct 21;4(10):e7543.
BACKGROUND: Political elections are dominance competitions. When men win a dominance competition, their testosterone levels rise or remain stable to resist a circadian decline; and when they lose, their testosterone levels fall. However, it is unknown whether this pattern of testosterone change extends beyond interpersonal competitions to the vicarious experience of winning or losing in the context of political elections. Women's testosterone responses to dominance competition outcomes are understudied, and to date, a clear pattern of testosterone changes in response to winning and losing dominance competitions has not emerged.
Subtypes of GABAergic neurons project axons in the neocortex
Higo S, Akashi K, Sakimura K, Tamamaki N.
Kyushu University of Nursing and Social Welfare Kumamoto, Japan.
Front Neuroanat. 2009;3:25.
gamma-aminobutyric acid (GABA)ergic neurons in the neocortex have been regarded as interneurons and speculated to modulate the activity of neurons locally. Recently, however, several experiments revealed that neuronal nitric oxide synthase (nNOS)-positive GABAergic neurons project cortico-cortically with long axons. In this study, we illustrate Golgi-like images of the nNOS-positive GABAergic neurons using a nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) reaction and follow the emanating axon branches in cat brain sections. These axon branches projected cortico-cortically with other non-labeled arcuate fibers, contra-laterally via the corpus callosum and anterior commissure.
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Kyushu University of Nursing and Social Welfare Kumamoto, Japan.
Front Neuroanat. 2009;3:25.
gamma-aminobutyric acid (GABA)ergic neurons in the neocortex have been regarded as interneurons and speculated to modulate the activity of neurons locally. Recently, however, several experiments revealed that neuronal nitric oxide synthase (nNOS)-positive GABAergic neurons project cortico-cortically with long axons. In this study, we illustrate Golgi-like images of the nNOS-positive GABAergic neurons using a nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) reaction and follow the emanating axon branches in cat brain sections. These axon branches projected cortico-cortically with other non-labeled arcuate fibers, contra-laterally via the corpus callosum and anterior commissure.
NO signaling in the CNS: from the physiological to the pathological
Bishop A, Anderson JE.
Department of Biological Sciences, University of Alabama at Huntsville, Huntsville, Alabama, USA.
Toxicology. 2005 Mar 15;208(2):193-205.
Nitric oxide (NO) is a free radical gas that has a Janus nature. As indicated by the literature and by our studies, in the cell, NO can either function as a beneficial physiological agent utilized for essential functions such as differentiation or neurotransmission, or as a pathological agent that causes or exacerbates central nervous system (CNS) disease and injury. Whether NO is helpful or harmful depends on a variety of factors, such as the cellular environment in which NO is released, the rate of NO flux, as determined by which NOS isozyme is activated, and what array of second messenger cascades are available for utilization by NO for beneficial or toxic cell signalling.
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Department of Biological Sciences, University of Alabama at Huntsville, Huntsville, Alabama, USA.
Toxicology. 2005 Mar 15;208(2):193-205.
Nitric oxide (NO) is a free radical gas that has a Janus nature. As indicated by the literature and by our studies, in the cell, NO can either function as a beneficial physiological agent utilized for essential functions such as differentiation or neurotransmission, or as a pathological agent that causes or exacerbates central nervous system (CNS) disease and injury. Whether NO is helpful or harmful depends on a variety of factors, such as the cellular environment in which NO is released, the rate of NO flux, as determined by which NOS isozyme is activated, and what array of second messenger cascades are available for utilization by NO for beneficial or toxic cell signalling.
Differential sensitivity of oligodendrocytes and motor neurons to reactive nitrogen species: implications for multiple sclerosis
Bishop A, Hobbs KG, Eguchi A, Jeffrey S, Smallwood L, Pennie C, Anderson J, Estévez AG.
Department of Biological Sciences, University of Alabama in Huntsville, Huntsville, Alabama, USA.
J Neurochem. 2009 Apr;109(1):93-104.
Depending on its concentration, nitric oxide (NO) has beneficial or toxic effects. In pathological conditions, NO reacts with superoxide to form peroxynitrite, which nitrates proteins forming nitrotyrosine residues (3NY), leading to loss of protein function, perturbation of signal transduction, and cell death. 3NY immunoreactivity is present in many CNS diseases, particularly multiple sclerosis. Here, using the high flux NO donor, spermine-NONOate, we report that oligodendrocytes are resistant to NO, while motor neurons are NO sensitive.
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Department of Biological Sciences, University of Alabama in Huntsville, Huntsville, Alabama, USA.
J Neurochem. 2009 Apr;109(1):93-104.
Depending on its concentration, nitric oxide (NO) has beneficial or toxic effects. In pathological conditions, NO reacts with superoxide to form peroxynitrite, which nitrates proteins forming nitrotyrosine residues (3NY), leading to loss of protein function, perturbation of signal transduction, and cell death. 3NY immunoreactivity is present in many CNS diseases, particularly multiple sclerosis. Here, using the high flux NO donor, spermine-NONOate, we report that oligodendrocytes are resistant to NO, while motor neurons are NO sensitive.
Mitigation of peroxynitrite-mediated nitric oxide (NO) toxicity as a mechanism of induced adaptive NO resistance in the CNS
Bishop A, Gooch R, Eguchi A, Jeffrey S, Smallwood L, Anderson J, Estevez AG.
Department of Biological Sciences, University of Alabama at Huntsville, Huntsville, Alabama, USA.
J Neurochem. 2009 Apr;109(1):74-84.
During CNS injury and diseases, nitric oxide (NO) is released at a high flux rate leading to formation of peroxynitrite (ONOO(*)) and other reactive nitrogenous species, which nitrate tyrosines of proteins to form 3-nitrotyrosine (3NY), leading to cell death. Previously, we have found that motor neurons exposed to low levels of NO become resistant to subsequent cytotoxic NO challenge; an effect dubbed induced adaptive resistance (IAR). Here, we report IAR mitigates, not only cell death, but 3NY formation in response to cytotoxic NO.
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Department of Biological Sciences, University of Alabama at Huntsville, Huntsville, Alabama, USA.
J Neurochem. 2009 Apr;109(1):74-84.
During CNS injury and diseases, nitric oxide (NO) is released at a high flux rate leading to formation of peroxynitrite (ONOO(*)) and other reactive nitrogenous species, which nitrate tyrosines of proteins to form 3-nitrotyrosine (3NY), leading to cell death. Previously, we have found that motor neurons exposed to low levels of NO become resistant to subsequent cytotoxic NO challenge; an effect dubbed induced adaptive resistance (IAR). Here, we report IAR mitigates, not only cell death, but 3NY formation in response to cytotoxic NO.