Abstract
This study determined whether macrophage inflammatory protein-1 β (MIP-1 β) plays a role in the hyperthermia caused by prostaglandin E 2 (PGE 2) given intracerebroventricularly (i.c.v.) in the rat. In these experiments, anti-murine MIP-1 β antibody (anti-MIP-1 β) was micro-injected in the anterior hypothalamic, preoptic area (AH/POA) just before i.c.v. PGE 2. The results showed that anti-MIP-1 β failed to alter the PGE 2 hyperthermia. However, immunocytochemical studies revealed MIP-1 β immunoreactivity detectable in both the organum vasculosum laminae terminalis (OVLT) and AH/POA in the febrile rat. These data thus demonstrate that MIP-1 β is sequestered in diencephalic structures underlying thermoregulation even though it is not involved in PGE 2 hyperthermia. This dissociation supports the viewpoint that at least two distinct systems exist in the brain which underlie a febrile response: MIP-1 β underlies one component whereas PGE 2 comprises the other.
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