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noradrenaline/atròfia
L'enllaç es desa al porta-retalls
Pàgina 1 des de 504 resultats
Potentiation of parkinsonian symptoms by depletion of locus coeruleus noradrenaline in 6-hydroxydopamine-induced partial degeneration of substantia nigra in rats.
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Parkinson's disease is characterized not only by a progressive loss of dopaminergic neurons in the substantia nigra but also by a degeneration of locus coeruleus noradrenergic neurons. The present study addresses the question of whether a partial neurodegeneration of dopaminergic neurons using
Degeneration of sympathetic nerves in vitro and development of smooth muscle supersensitivity to noradrenaline.
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1. The sequence of events involved in degeneration of sympathetic nerve terminals has been studied in vitro in the expansor secundariorum muscle of the chicken.2. The muscle underwent a degeneration contraction due to abrupt release of noradrenaline stores from the nerves about 18 hr after
Degeneration release of noradrenaline in skin flaps in rats.
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To study if noradrenaline released from degenerating sympathetic nerves may contribute to metabolic stimulation and low blood flow in an experimental skin flap, we have determined noradrenaline levels in such skin flaps. Attempts to use radioenzymatic methodology for the determination of
Degeneration secretion and noradrenaline disappearance in rat salivary glands following proximal or distal axotomy.
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The noradrenaline (NA) content and the degeneration secretion of saliva were studied in rat salivary glands, following proximal or distal sympathetic denervation. Proximal denervation was obtained by removal of the cervical superior ganglion, which left a long stump of adrenergic axons attached to
Reduction of noradrenaline in cerebellum of patients with olivopontocerebellar atrophy.
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Noradrenaline (NA) was measured in postmortem cerebellar cortex of 15 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The mean cerebellar cortical NA level was significantly reduced (by 40%) in OPCA as compared with control values. The NA deficit most likely reflects a
Ca2+ dependence of the release of noradrenaline during nerve degeneration in the parotid gland.
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Amylase secretion "in vitro" was used as an indication of the degeneration activity of sympathetically denervated parotid glands. Seventeen and a half hours after sympathetic denervation, slices of parotid gland released amylase into the incubation medium at a rate higher than that observed for
The neurotransmitter noradrenaline rescues septal cholinergic neurons in culture from degeneration caused by low-level oxidative stress.
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We have developed a model system in which rat basal forebrain cholinergic neurons degenerate progressively when maintained in culture conditions that make them susceptible to low-level oxidative stress. In this study, we showed that cholinergic neurons identified by acetylcholinesterase
Noradrenaline neuron degeneration contributes to motor impairments and development of L-DOPA-induced dyskinesia in a rat model of Parkinson's disease.
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Parkinson's disease (PD) is characterized by progressive loss of dopaminergic (DA) neurons in the substantia nigra. However, studies of post-mortem PD brains have shown that not only DA neurons but also the noradrenergic (NA) neurons in the locus coeruleus degenerate, and that the NA
Age- and α-Synuclein-Dependent Degeneration of Dopamine and Noradrenaline Neurons in the Annual Killifish Nothobranchius furzeri.
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Parkinson's disease (PD) is a neurodegenerative disease characterized by α-synuclein-positive inclusion bodies and loss of neurons, including dopaminergic neurons. Difficulty in replicating PD phenotypes using animal models partly limits the understanding of PD and the therapy required. Although PD
Release of a smooth-muscle-active substance besides noradrenaline from degenerating sympathetic terminals in the rabbit eye.
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Degeneration of central and peripheral noradrenaline neurons produced by 6-hydroxy-DOPA.
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Selective 6-hydroxy-DOPA induced degeneration of central and peripheral noradrenaline neurons.
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The cause of the supersensitivity of smooth muscle to noradrenaline after sympathetic degeneration.
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Pharmacological modifications of the 6-hydroxy-dopa induced degeneration of central noradrenaline neurons.
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On the specificity of 6-hydroxydopamine-induced degeneration of central noradrenaline neurons after intracerebral injection.
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