期刊
BRAIN RESEARCH
卷 1019, 期 1-2, 页码 162-169出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2004.06.016
关键词
orexin; lateral hypothalamus; wakefulness; neurodegeneration; rat
资金
- NIA NIH HHS [AG09975, AG15853] Funding Source: Medline
- NIMH NIH HHS [MH55772] Funding Source: Medline
- NINDS NIH HHS [NS30140] Funding Source: Medline
The number of hypocretin-containing neurons is markedly decreased in most patients with the sleep disorder narcolepsy. It is presently not known why the loss of hypocretin neurons occurs in these patients. In the present study, we tested the role of inflammation in the degeneration of hypocretin neurons. The proinflammagen lipopolysaccharide (LPS) was infused chronically for 30 days (flow rate 0.22 mug/h) into the lateral hypothalamus in rats. Compared with chronic infusions of phosphate-buffered saline (PBS), LPS infusions produced a decline in the number of hypocretin (29.7% reduction), melanin concentrating hormone (MCH; 24.7% reduction), and neuronal nuclear antigen (NeuN)-immunoreactive neurons, as well as a dense distribution of reactive astrocytes and microglia within the lateral hypothalamus. LPS infusions also produced a large increase in the amounts of wakefulness 6 days after the onset of infusion (72.5 +/- 8.7% of wakefulness during lights-on period compared with 45.3 +/- 1.8% in PBS-treated rats). Amounts of wakefulness returned to control levels in all LPS-treated rats 30 days after the onset of infusion. A single injection of LPS (1, 5, or 10 mug) did not produce a significant decline in the number of hypocretin, MCH, or NeuN-positive neurons. The loss of hypocretin neurons produced by chronic LPS administration suggests that inflammation may play a role in the loss of hypocretin neurons in narcolepsy. (C) 2004 Elsevier B.V. All rights reserved.
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