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

• DOI: 10.1523/jneurosci.20-01-00149.2000
• Publication Date: 2018-04-04T20:40:32Z
• Authors: Yuekui Li; Ling Liu; Jinsong Kang; Jin G. Sheng; Steven W. Barger; Robert E. Mrak; W. Sue T. Griffin
• Keywords: Male; Neurons; Brain; Glutamic Acid; Cell Communication; PC12 Cells; Gene Expression Regulation, Enzymologic; Choline O-Acetyltransferase; Rats; 3. Good health; Rats, Sprague-Dawley; Amyloid beta-Protein Precursor; 03 medical and health sciences; 0302 clinical medicine; Alzheimer Disease; Acetylcholinesterase; Animals; Microglia; RNA, Messenger; Interleukin-1

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