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asphyxia neonatorum/tyrosine
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Perinatal asphyxia induces region-specific long-term changes in mRNA levels of tyrosine hydroxylase and dopamine D(1) and D(2) receptors in rat brain.
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To study the effects of neonatal asphyxia on gene expression of the dopaminergic systems, we determined quantitatively the mRNA levels of tyrosine hydroxylase, dopamine transporter, dopamine D(1) and D(2) receptors in substantia nigra/ventral tegmental area, striatum and limbic area. The mRNA levels
Perinatal asphyxia-induced changes in rat brain tyrosine hydroxylase-immunoreactive cell body number: effects of nicotine treatment.
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Perinatal asphyxia (15-22 min) was induced to male Sprague-Dawley rat pups during the last day of gestation and the surviving pups were sacrificed at 4 weeks of age. Brain sections were stained for tyrosine hydroxylase immunoreactivity and Cresyl violet. With increasing duration of perinatal
Effect of perinatal asphyxia on tyrosine hydroxylase and D2 and D1 dopamine receptor mRNA levels expressed during early postnatal development in rat brain.
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This study was designed to investigate the postnatal developmental plasticity of the mesostriatal and mesolimbic dopamine systems that occurs following perinatal asphyxia. The time course and patterning of the changes in levels of tyrosine hydroxylase (TH), and D1 and D2 dopamine receptor (R) mRNA
Neonatal asphyxia induces the nitration of cardiac myosin light chain 2 that is associated with cardiac systolic dysfunction.
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Hypoxia followed by reoxygenation (H-R) observed during perinatal asphyxia is a serious complication with high mortality and morbidity rates that may cause adverse cardiovascular effects in neonates. Our aim was to determine if oxidative stress related to H-R induces peroxynitrite-dependent
Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia in the rat.
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Perinatal asphyxia (PA) is considered to lead to a variety of brain disorders including spasticity, epilepsy, mental retardation, and minimal brain disorder syndromes and may form the basis for psychiatric and neurodegenerative diseases later in life. We examined markers for neuronal transmission
Perinatal asphyxia increases bFGF mRNA levels and DA cell body number in the mesencephalon of rats.
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The present investigation was undertaken in order to study the long-term effects of perinatal asphyxia on basic fibroblast growth factor (bFGF) gene expression and the number of dopamine nerve cell bodies in the mesencephalon of the rat. Asphyxia was induced during birth for 19-20 min. A 30%
Perinatal asphyxia impairs connectivity and dopamine neurite branching in organotypic triple culture from rat substantia nigra, neostriatum and neocortex.
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The effect of perinatal asphyxia on brain development was studied with organotypic cultures from substantia nigra, neostriatum and neocortex. Asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Following asphyxia, the
Decrease of brain protein kinase C, protein kinase A, and cyclin-dependent kinase correlating with pH precedes neuronal death in neonatal asphyxia.
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BACKGROUND
Acidosis, energy depletion, overstimulation by excitatory amino acids, and free radical-mediated reactions are the major, current concepts for the explanation of damage and death resulting from asphyxia. Impaired protein phosphorylation by protein kinase C represents another mechanism
Plasticity of the central nervous system (CNS) following perinatal asphyxia: does nicotinamide provide neuroprotection?
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We have investigated the idea that nicotinamide, a non-selective inhibitor of the sentinel enzyme Poly(ADP-ribose) polymerase-I (PARP-1), provides neuroprotection against the long-term neurological changes induced by perinatal asphyxia. Perinatal asphyxia was induced in vivo by immersing
A combined behavioral and morphological study on the effects of fetal asphyxia on the nigrostriatal dopaminergic system in adult rats.
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Fetal asphyxic insults in the brain are known to be associated with developmental neurological problems like neuromotor disorders. However, little is known about the long-term consequences of fetal asphyxia (FA). For that reason, the present study investigated the long-term effects of FA on motor
Effects of perinatal asphyxia on cell survival, neuronal phenotype and neurite growth evaluated with organotypic triple cultures.
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The effect of perinatal asphyxia on brain development was studied with organotypic cultures from substantia nigra, neostriatum and neocortex. Asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Following asphyxia, the
Effects of perinatal asphyxia on the mesostriatal/mesolimbic dopamine system of neonatal and 4-week-old male rats.
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The present study was undertaken in order to study the effects of perinatal asphyxia on tyrosine hydroxylase (TH) activity, dopamine levels and turnover, and dopamine metabolites (3,4-dihydroxyphenylacetic acid, DOPAC, homovanillic acid, HVA, and 3-methoxytyramine, 3-MT, analyzed by high-performance
Nicotine treatment counteracts perinatal asphyxia-induced changes in the mesostriatal/limbic dopamine systems and in motor behaviour in the four-week-old male rat.
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In the present study, the effects of nicotine treatment on the changes induced by perinatal asphyxia in exploratory and D-amphetamine-induced behaviour, and in the number of brain tyrosine hydroxylase-immunoreactive nerve cell bodies were investigated in four-week-old male rats. Asphyxia was induced
Plasticity of basal ganglia neurocircuitries following perinatal asphyxia: effect of nicotinamide.
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The potential neuroprotection of nicotinamide on the consequences of perinatal asphyxia was investigated with triple organotypic cultures. Perinatal asphyxia was induced in vivo by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Sibling
Long-term effect of moderate and profound hypothermia on morphology, neurological, cognitive and behavioural functions in a rat model of perinatal asphyxia.
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BACKGROUND
Perinatal asphyxia is a frequent cause of neurological handicap with no known therapy. However, hypothermic therapy has recently attracted attention owing to its neuroprotective property in brain of immature organisms.
OBJECTIVE
Hypothermia appears to be promising in reversing the
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