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ARTICLE, Cellular/Molecular

Neuronal–Glial Interactions Mediated by Interleukin-1 Enhance Neuronal Acetylcholinesterase Activity and mRNA Expression

Yuekui Li, Ling Liu, Jinsong Kang, Jin G. Sheng, Steven W. Barger, Robert E. Mrak and W. Sue T. Griffin
Journal of Neuroscience 1 January 2000, 20 (1) 149-155; DOI: https://doi.org/10.1523/JNEUROSCI.20-01-00149.2000
Yuekui Li
1Donald W. Reynolds Department of Geriatrics and the Departments of
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Ling Liu
1Donald W. Reynolds Department of Geriatrics and the Departments of
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Jinsong Kang
1Donald W. Reynolds Department of Geriatrics and the Departments of
9Department of Pathophysiology, Norman Bethune University of Medical Sciences, Changchun 130021, People's Republic of China
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Jin G. Sheng
1Donald W. Reynolds Department of Geriatrics and the Departments of
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Steven W. Barger
1Donald W. Reynolds Department of Geriatrics and the Departments of
2Anatomy,
6the Geriatric Research, Education, Clinical Center,
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Robert E. Mrak
2Anatomy,
3Pathology,
8Pathology Service, McClellan Memorial Veterans Affairs Medical Center, Little Rock, Arkansas 72205, and
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W. Sue T. Griffin
1Donald W. Reynolds Department of Geriatrics and the Departments of
2Anatomy,
4Medicine, and
5Psychiatry, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205,
6the Geriatric Research, Education, Clinical Center,
7Mental Illness Research Education and Clinical Center, and
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Abstract

Cholinergic dysfunction in Alzheimer's disease has been attributed to stress-induced increases in acetylcholinesterase (AChE) activity. Interleukin-1 (IL-1) is overexpressed in Alzheimer's disease, and stress-related changes in long-term potentiation, an ACh-related cerebral function, are triggered by interleukin-1. Microglial cultures (N9) synthesized and released IL-1 in response to conditioned media obtained from glutamate-treated primary neuron cultures or PC12 cells. This conditioned media contained elevated levels of secreted β-amyloid precursor protein (sAPP). Naive PC12 cells cocultured with stimulated N9 cultures showed increased AChE activity and mRNA expression. These effects on AChE expression and activity could be blocked by either preincubating the glutamate-treated PC12 supernatants with anti-sAPP antibodies or preincubating naive PC12 cells with IL-1 receptor antagonist. These findings were confirmed in vivo; IL-1-containing pellets implanted into rat cortex also increased AChE mRNA levels. Neuronal stress in Alzheimer's disease may induce increases in AChE expression and activity through a molecular cascade that is mediated by sAPP-induced microglial activation and consequent overexpression of IL-1.

  • acetylcholinesterase
  • Alzheimer's disease
  • β-amyloid precursor protein
  • choline acetyltransferase
  • cholinergic systems
  • interleukin-1
  • neuronal cultures
  • neuronal stress
  • PC12 cells
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The Journal of Neuroscience: 20 (1)
Journal of Neuroscience
Vol. 20, Issue 1
1 Jan 2000
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Neuronal–Glial Interactions Mediated by Interleukin-1 Enhance Neuronal Acetylcholinesterase Activity and mRNA Expression
Yuekui Li, Ling Liu, Jinsong Kang, Jin G. Sheng, Steven W. Barger, Robert E. Mrak, W. Sue T. Griffin
Journal of Neuroscience 1 January 2000, 20 (1) 149-155; DOI: 10.1523/JNEUROSCI.20-01-00149.2000

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Neuronal–Glial Interactions Mediated by Interleukin-1 Enhance Neuronal Acetylcholinesterase Activity and mRNA Expression
Yuekui Li, Ling Liu, Jinsong Kang, Jin G. Sheng, Steven W. Barger, Robert E. Mrak, W. Sue T. Griffin
Journal of Neuroscience 1 January 2000, 20 (1) 149-155; DOI: 10.1523/JNEUROSCI.20-01-00149.2000
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Keywords

  • acetylcholinesterase
  • Alzheimer's disease
  • β-amyloid precursor protein
  • choline acetyltransferase
  • cholinergic systems
  • interleukin-1
  • neuronal cultures
  • neuronal stress
  • PC12 cells

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