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Cortical cell death induced by IL-1 is mediated via actions in the hypothalamus of the rat.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Allan, S. M. Rothwell, N. J. Parker, L. C. Davies, R. Luheshi, G. N. Collins, B.
Description	Author Affiliation: Allan SM ( School of Biological Sciences, 1.124 Stopford Building, University of Manchester, Oxford Road, Manchester, M13 9PT, United Kingdom.);
Abstract	The cytokine IL-1 mediates diverse forms of neurodegeneration, but its mechanism of action is unknown. We have demonstrated previously that exogenous and endogenous IL-1 acts specifically in the rat striatum to dramatically enhance ischemic and excitotoxic brain damage and cause extensive cortical injury. Here we tested the hypothesis that this distant effect of IL-1 is mediated through polysynaptic striatal outputs to the cortex via the hypothalamus. We show that IL-1beta injected into the rat striatum with the excitotoxin alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (S-AMPA) caused increased expression of IL-1beta (mRNA and protein) mainly in the cortex where maximum injury occurs. Marked increases in IL-1beta mRNA and protein were also observed in the hypothalamus. S-AMPA, injected alone into the striatum, caused only localized damage, but administration of IL-1beta into either the striatum or the lateral hypothalamus immediately after striatal S-AMPA resulted in widespread cell loss throughout the ipsilateral cortex. Finally we showed that the cortical cell death produced by striatal coinjection of S-AMPA and IL-1beta was significantly reduced by administration of the IL-1 receptor antagonist into the lateral hypothalamus. These data suggest that IL-1beta can act in the hypothalamus to modify cell viability in the cortex. We conclude that IL-1-dependent pathways project from the striatum to the cortex via the hypothalamus and lead to cortical injury, and that these may contribute to a number of human neurological conditions including stroke and head trauma.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	10
Volume Number	97
Language	English
Publisher	National Academy of Sciences
Publisher Date	2000-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cerebral Cortex Pathology Hypothalamus Immunology Interleukin-1 Genetics Toxicity Neurons Alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Animals Drug Effects Corpus Striatum Interleukin 1 Receptor Antagonist Protein Kinetics Models, Neurological Rats, Sprague-Dawley Recombinant Proteins Pharmacology Reverse Transcriptase Polymerase Chain Reaction Sialoglycoproteins Time Factors Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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