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norepinephrine/atrofia
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Norepinephrine metabolism in the cerebellum of the purkinje cell degeneration (pcd) mutant mouse.
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Norepinephrine (NE) metabolism in brain regions was studied in the Purkinje cell degeneration (pcd) mutant mouse. The Purkinje cells, which are target cells for noradrenergic (NA) neurons, degenerate completely in the pcd mutant mouse between 17 and 45 days of age, but the NA terminals remain
Elevated norepinephrine may be an etiological factor in a wide range of diseases: age-related macular degeneration, systemic lupus erythematosus, atrial fibrillation, metabolic syndrome.
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The neurotransmitter norepinephrine (NE) participates in a broad range of physiological functions, both in the brain and in the periphery, where it is a principal output molecule of the sympathetic nervous system. NE receptors are present in nearly all, if not all, organs of the body, which may
Effects of AM281, a cannabinoid antagonist, on circulatory deterioration and cytokine production in an endotoxin shock model: comparison with norepinephrine.
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OBJECTIVE
The purpose of this study was to examine the comparative effects of AM281, a cannabinoid antagonist, and norepinephrine (NE) on systemic hemodynamics, and renal and mesenteric artery blood flow in an endotoxin shock model.
METHODS
The study was designed to include two sets of experiments:
Cerebrospinal fluid norepinephrine, 3-methoxy-4-hydroxyphenylglycol and neuropeptide Y levels in Parkinson's disease, multiple system atrophy and dementia of the Alzheimer type.
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Neuropeptide Y, one of the most abundant polypeptides within the nervous system, is co-stored with catecholamines, especially norepinephrine (NE), thus suggesting its possible involvement in pathologies characterized by a noradrenergic impairment. In Parkinson's disease (PD), as well as in multiple
Nerve terminal degeneration in the rat iris observed following chronic topical 2% epinephrine and 0.1% dipivalyl epinephrine: a quantitative comparison of electron microscopic observations and tissue norepinephrine levels.
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This is the first report of nerve terminal degeneration within the iris following topical dipivalyl epinephrine 0.1% treatment. A quantitative comparison of the effects of topically applied epinephrine 2%, dipivalyl epinephrine 0.1%, and placebo vehicle on the nerve terminals within the iris of a
Degeneration mydriasis and hyperemia of the iris after superior cervical ganglionectomy in the rabbit. Evidence for release of more than norepinephrine during degeneration of adrenergic terminals.
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Cerebrospinal fluid norepinephrine reductions in man after degeneration and electrical stimulation of the caudate nucleus.
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Norepinephrine reductions in cerebrospinal fluid in man after electrical stimulation and degeneration of the caudate nucleus.
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Changes in neuronal uptake and metabolism of, and sensitivity to, norepinephrine during the degeneration secretion in the rat submaxillary gland.
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Degeneration of nerve terminals in cats following systemic epinephrine: depletion of tissue norepinephrine correlated with ultrastructural changes.
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Degeneration release of norepinephrine causes transient ocular hyperemia mediated by prostaglandins.
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A low dose of xylamine produces sustained and selective decreases in rat brain norepinephrine without evidence of neuronal degeneration.
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The effects of a chronic partial depletion of rat cortical NE by a single dose of xylamine (20 mg/kg i.p.) on pre- and postsynaptic noradrenergic functionality were studied 4 hr, 14, 21 and 35 days after treatment. This dose of xylamine resulted in a 40 to 50% selective decrease in cortical levels
Effect of 6-hydroxydopamine on brain norepinephrine and dopamine evidence for selective degeneration of catecholamine neurons.
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Locus Coeruleus Degeneration Induces Forebrain Vascular Pathology in a Transgenic Rat Model of Alzheimer's Disease.
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Noradrenergic locus coeruleus (LC) neuron loss is a significant feature of mild cognitive impairment and Alzheimer's disease (AD). The LC is the primary source of norepinephrine in the forebrain, where it modulates attention and memory in vulnerable cognitive regions such as prefrontal cortex (PFC)
Reduced vesicular storage of catecholamines causes progressive degeneration in the locus ceruleus.
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Parkinson's disease (PD) is the most common neurodegenerative motor disease. Pathologically, PD is characterized by Lewy body deposition and subsequent death of dopamine neurons in the substantia nigra pars compacta. PD also consistently features degeneration of the locus ceruleus, the main source
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