Amyloid 1-42 peptide alters the gating of human and mouse -bungarotoxin-sensitive nicotinic receptors
نویسندگان
چکیده
منابع مشابه
beta-Amyloid(1-42) peptide directly modulates nicotinic receptors in the rat hippocampal slice.
Alzheimer's disease (AD) is a human neurological disorder characterized by an increasing loss of cognitive function and the presence of extracellular neuritic plaques composed of the beta-amyloid peptide (Abeta(1-42)). However, the link between these molecular correlates of AD and the loss of cognitive function has not been established. The pathology associated with AD includes the loss of basa...
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Emerging evidence indicates that amyloid peptide (A ) initially induces subtle alterations in synaptic function in Alzheimer disease.We have recently shown that A binds to 2 adrenergic receptor ( 2AR) and activates protein kinase A (PKA) signaling for glutamatergic regulation of synaptic activities. Here we show that in the cerebrums of mice expressing human familial mutant presenilin 1 and amy...
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The Alzheimer’s disease pathogenic peptide, -amyloid42 (A 42), induces tau protein phosphorylation. Because hyperphosphorylated tau is a consistent component of neurofibrillary tangles, a pathological hallmark of Alzheimer’s disease, we investigated the signaling molecules involved in A 42-induced tau phosphorylation. We show that A 42 elicited rapid and reversible tau protein phosphorylation o...
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We assessed the pharmacological activity of anabaseine, a toxin found in certain animal venoms, relative to nicotine and anabasine on a variety of vertebrate nicotinic receptors, using cultured cells, the Xenopus oocyte expression system, contractility assays with skeletal and smooth muscle strips containing nicotinic receptors and in vivo rat prostration assay involving direct injection into t...
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ژورنال
عنوان ژورنال: The Journal of Physiology
سال: 2003
ISSN: 0022-3751
DOI: 10.1113/jphysiol.2002.035436