Cited by 74Nerve injury and regenerationNeurological Disorders and TreatmentsNeuroinflammation and Neurodegeneration Mechanisms

Niacin treatment of stroke increases synaptic plasticity and axon growth in rats

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Cui, Xu, Chopp, Michael, Zacharek, Alex, Roberts, Cynthia, Buller, Benjamin, Ion, Madalina, Chen, Jieli·2010·Stroke

Abstract

Background and Purpose— Niacin is the most effective medication in current clinical use for increasing high-density lipoprotein cholesterol. We tested the hypothesis that niacin treatment of stroke promotes synaptic plasticity and axon growth in the ischemic brain. Methods— Male Wistar rats were subjected to 2 hours of middle cerebral artery occlusion and treated with or without Niaspan (a prolonged-release formulation of niacin, 40 mg/kg) daily for 14 days starting 24 hours after middle cerebral artery occlusion. The expression of synaptophysin, Nogo receptor, Bielschowsky silver, brain-derived neurotrophic factor, and its receptor tropomyosin-related kinase B were measured by immunohistostaining and Western blot, respectively, in the ischemic brain. Complementing in vivo studies, primary cultured neurons were used to test the effect of niacin and high-density lipoprotein on neurite outgrowth and brain-derived neurotrophic factor/tropomyosin-related kinase B expression. Results— Niaspan treatment of stroke significantly increased synaptophysin, Bielschowsky silver, brain-derived neurotrophic factor/tropomyosin-related kinase B expression, and decreased Nogo receptor expression in the ischemic brain compared with middle cerebral artery occlusion control animals ( P <0.05, n=8/group). Niacin and high-density lipoprotein treatment significantly increased neurite outgrowth and brain-derived neurotrophic factor/tropomyosin-related kinase B expression in primary cultured neurons. Tropomyosin-related kinase B inhibitor attenuated niacin-induced neurite outgrowth ( P <0.05, n=6/group). Conclusions— Niacin treatment of stroke promotes synaptic plasticity and axon growth, which is mediated, at least partially, by the brain-derived neurotrophic factor/tropomyosin-related kinase B pathways.

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Crossref · 10.1161/strokeaha.110.589333

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Authors
Cui, X., Chopp, M., Zacharek, A., Roberts, C., Buller, B., Ion, M., & Chen, J.
Affiliations
Henry Ford Health (US)
Venue
Stroke
Published
2010-09
Volume
41
Issue
9
Pages
2044-2049
ISSN
  • 0039-2499 (ISSN-L)
  • 1524-4628
OpenAlex
W2160479657
Cited by
74
References
33
Citations by year
2026: 1 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 8 · 2018: 5 · 2017: 2 · 2016: 4 · 2015: 5 · 2014: 10 · 2013: 4 · 2012: 8
FWCI
1.94
Type
journal article
Language
en
Open access
Locations
  • Stroke (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG031811)
  • National Institute of Neurological Disorders and Stroke (P01NS23393, P01NS023393, R41NS064708)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
nicotinic acid, Niaspan, ischemic brain, synaptic plasticity, axon growth, neurite outgrowth, brain-derived neurotrophic factor, Nogo receptor, high-density lipoprotein, middle cerebral artery occlusion, synaptophysin, neuroprotection
MeSH terms
Nogo Receptor 1, Analysis of Variance, Animals, Axons, Cells, Cultured, Immunohistochemistry, Male, Myelin Proteins, Neuronal Plasticity, Neurons, Niacin, Receptors, Cell Surface, Blotting, Western, Synaptophysin, Rats, Wistar, Receptors, Peptide, Brain-Derived Neurotrophic Factor, Reverse Transcriptase Polymerase Chain Reaction, Stroke, Receptor, trkB, Rats, GPI-Linked Proteins

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