Cited by 41Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

Neurotoxicity of Aβ amyloid protein in vitro is not altered by calcium channel blockade

Whitson, J.S., Appel, S.H.·1995·Neurobiology of Aging

Abstract

In cortical cultures, A beta protein destabilizes calcium homeostasis, but direct neurotoxicity of A beta is not observed. In hippocampal cultures, we and others find treatment with A beta protein decreases neuronal survival, but the mechanism of neurotoxicity is unknown. We have used low-density, serum-free cultures of hippocampal neurons to determine whether the neurotoxicity of A beta protein in vitro can be altered by voltage- or ligand-gated calcium channel antagonists or cyclic nucleotides. In these cultures, neither omega-conotoxin, nifedipine, verapamil, APV, nor MK-801 altered the survival of neurons exposed to synthetic A beta 1-40. The N-channel antagonist diltiazem decreased A beta 1-40 toxicity repeatedly, but slightly, perhaps by indirectly contributing to increased neuronal viability. Treatment of cultures with dibutyryl cAMP, 8-bromo cAMP, dibutyryl cGMP, and 8-bromo cGMP also failed to alter A beta toxicity. Thus, the toxicity of beta protein in low-density hippocampal cultures was not directly altered either by calcium channel blockers or by the addition of cyclic nucleotides.

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Crossref · 10.1016/0197-4580(95)80002-9

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  • Results from recent studies assessing the impact of aging on hippocampal and other temporal lobe structures have been variable: some found age-related declines in volume in normal elderly individuals, while others did not.

    “Results from recent studies assessing the impact of aging on hippocampal and other temporal lobe structures have been variable. Some have found age-related declines in volume in normal elderly individuals [4, 30, 31] while others have not [3, 32].”

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Authors
Whitson, J. S., & Appel, S. H.
Affiliations
Baylor College of Medicine (US)
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
1995-01
Volume
16
Issue
1
Pages
5-10
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2037639183
Cited by
41
References
33
Citations by year
2020: 1 · 2013: 3 · 2012: 1
FWCI
4.21
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p50ag008664-09)
  • National Institute on Aging (AG00183, AG-08664)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid-beta, Aβ(1-40), neurotoxicity, calcium channel blockers, calcium homeostasis, hippocampal neurons, neuronal survival, diltiazem, omega-conotoxin, nifedipine, verapamil, APV, MK-801, cyclic nucleotides, Alzheimer's disease
MeSH terms
Cyclic AMP, Animals, Calcium Channel Blockers, Cell Survival, Cells, Cultured, Cyclic GMP, Hippocampus, Hydrolysis, Immunohistochemistry, Trypsin, Ion Channel Gating, Amyloid beta-Peptides, Tissue Fixation, Culture Media, Serum-Free, Rats, Sprague-Dawley, Rats

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