Abstract：
:This study determined whether macrophage inflammatory protein-1beta (MIP-1beta) plays a role in the hyperthermia caused by prostaglandin E2 (PGE2) given intracerebroventricularly (i.c.v.) in the rat. In these experiments, anti-murine MIP-1beta antibody (anti-MIP-1beta) was micro-injected in the anterior hypothalamic, preoptic area (AH/POA) just before i.c.v. PGE2. The results showed that anti-MIP-1beta failed to alter the PGE2 hyperthermia. However, immunocytochemical studies revealed MIP-1beta immunoreactivity detectable in both the organum vasculosum laminae terminalis (OVLT) and AH/POA in the febrile rat. These data thus demonstrate that MIP-1beta is sequestered in diencephalic structures underlying thermoregulation even though it is not involved in PGE2 hyperthermia. This dissociation supports the viewpoint that at least two distinct systems exist in the brain which underlie a febrile response: MIP-1beta underlies one component whereas PGE2 comprises the other.
journal_name
Brain Resjournal_title
Brain researchauthors
Armengol JA,Benamar K,Fernández-Alonso A,Sancibrián M,Myers RD,Miñano FJdoi
10.1016/s0006-8993(96)01362-5subject
Has Abstractpub_date
1997-02-14 00:00:00pages
245-9issue
1-2eissn
0006-8993issn
1872-6240pii
S0006-8993(96)01362-5journal_volume
748pub_type
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