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choline acetyltransferase/hypoxia
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 51 tuloksia
Heart-specific overexpression of choline acetyltransferase gene protects murine heart against ischemia through hypoxia-inducible factor-1α-related defense mechanisms.
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BACKGROUND
Murine and human ventricular cardiomyocytes rich in acetylcholine (Ach) receptors are poorly innervated by the vagus, compared with whole ventricular innervation by the adrenergic nerve. However, vagal nerve stimulation produces a favorable outcome even in the murine heart, despite
Ultrastructural localisation of substance P and choline acetyltransferase in endothelial cells of rat coronary artery and release of substance P and acetylcholine during hypoxia.
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Substance P and choline acetyltransferase have been localised in a small proportion of endothelial cells of rat coronary arteries using electron microscopic immunocytochemistry. During a hypoxic period of 1 min, coronary vasodilatation was produced in the Langendorff heart preparation and increased
Carbamylated erythropoietin ameliorates hypoxia-induced cognitive and behavioral defects with the generation of choline acetyltransferase-positive neurons.
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Carbamylated erythropoietin (CEPO) is attracting widespread interest because of its neuroprotective effects without influencing erythropoiesis. Here we show that CEPO, unlike EPO, does not stimulate erythropoiesis. Both CEPO and EPO inhibit the death/apoptosis of neurons in the hypoxic model of
Effects of postnatal hypoxia-ischemia on cholinergic neurons in the developing rat forebrain: choline acetyltransferase immunocytochemistry.
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We studied the effect of early postnatal hypoxia-ischemia on cholinergic neurons in the developing rat forebrain using immunohistochemistry for choline acetyltransferase (ChAT). In 7-day-old rat pups, hypoxia-ischemia was induced in one cerebral hemisphere by combining unilateral carotid ligation
Impaired spatial working memory and altered choline acetyltransferase (CHAT) immunoreactivity and nicotinic receptor binding in rats exposed to intermittent hypoxia during sleep.
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Exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered breathing (SDB), is associated with cognitive impairment, neurodegeneration, oxidative stress, and inflammatory responses within rodent brain regions such as the basal forebrain. In this region, damage to cholinergic neurons
The effect of hypoxia on neurotransmitter phenotype of forebrain cholinergic neurons.
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The effect of hypoxia on the neurotransmitter phenotype of rat forebrain cholinergic neurons was analyzed using a dissociated fetal rat culture system. The aims of this study were to examine the feasibility of using choline acetyltransferase (ChAT) activity as a measure of cell injury and/or
Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia.
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This study tested the hypothesis that during hypercapnia or hypoxia, airway-related vagal preganglionic neurons (AVPNs) of the nucleus ambiguus (NA) release acetylcholine (ACh), which in a paracrine fashion, activates ACh receptors expressed by inspiratory rhythm generating cells. AVPNs in the NA
Free chelatable zinc modulates the cholinergic function during hypobaric hypoxia-induced neuronal damage: an in vivo study.
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The deregulation of cholinergic system and associated neuronal damage is thought to be a major contributor to the pathophysiologic sequelae of hypobaric hypoxia-induced memory impairment. Uniquely, the muscarinic receptors also play a role in zinc uptake. Despite the potential role of muscarinic
Differential expression of calcitonin gene-related peptide (CGRP) and choline acetyltransferase (ChAT) in the axotomized motoneurons of normoxic and hypoxic rats.
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We employed a double injury model (axotomy along with hypoxia) to determine how nerve injury and hypoxic insult would affect the expression of calcitonin gene-related peptide (CGRP) and choline acetyltransferase (ChAT) in the hypoglossal nucleus (HN) and nucleus ambiguus (NA). Adult rats were
Hypoxia-induced changes in parasympathetic neurochemical markers in guinea pig heart.
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Exposure of animals to hypoxia produces cardiovascular changes including right ventricular hypertrophy and alterations in heart rate. The activity of choline acetyltransferase, a neurochemical marker of parasympathetic innervation, and the density of muscarinic cholinergic receptors, measured by the
Asymmetrical perfusion fixation in a rodent model of perinatal hypoxia-ischemia may lead to artifactual morphologic asymmetries.
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We have observed asymmetries in perfusion between the cerebral hemispheres in immature rats previously subjected to carotid ligation in a model of perinatal hypoxia-ischemia. These asymmetries are associated with marked differences in the number of neurons stained positive by immunoperoxidase
[Effects of hypoxia on the brain cholinergic system in the rat].
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Effects of mild hypoxic hypoxia on brain cholinergic system in the rat were investigated with choline acetyltransferase (CAT), acetylcholinesterase (AChE) and muscarinic acetylcholine receptor (MR) as indicators of cholinergic system. Hypoxic exposure of 10% oxygen concentration was undertaken for
Electrophysiological properties of laryngeal motoneurones in rats submitted to chronic intermittent hypoxia.
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CONCLUSIONS
The respiratory control of the glottis by laryngeal motoneurones is characterized by inspiratory abduction and post-inspiratory adduction causing decreases and increases in upper airway resistance, respectively. Chronic intermittent hypoxia (CIH), an important component of obstructive
The effect of neonatal hypoxia-ischemia on striatal cholinergic neuropil: a quantitative morphologic analysis.
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Little is known about the alterations in the neurochemical anatomy of the brain in the static encephalopathies of childhood, of which one cause is hypoxia-ischemia. We and others have previously shown in neonatal rodent that experimental hypoxia-ischemia results in an increase in the density of
Affected enzyme activities in Alzheimer's disease are sensitive to antemortem hypoxia.
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Many enzyme activities in Alzheimer's disease (AD) are changed. Some of these enzyme activities are related to certain neurotransmitter systems. Enzymes in the brain can also be sensitive to antemortem hypoxia. In the present study it was determined if enzyme activities that are altered in AD are
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