Transporter-mediated prostaglandin E₂ elimination across the rat blood-brain barrier and its attenuation by the activation of N-methyl-D-aspartate receptors.

Prostaglandin (PG) E2 is involved in neuroinflammation and neurotoxicity, and the cerebral PGE2 concentration is increased in neurodegenerative diseases. Because the intracerebral concentration of L-glutamate (L-Glu) is reported to be also elevated in neurodegenerative diseases, it has been proposed that L-Glu affects PGE2 dynamics in the brain, and thus exacerbates neural excitotoxicity. The purpose of this study was to investigate the effect of intracerebral L-Glu on PGE2 elimination across the blood-brain barrier (BBB) in rats by using the intracerebral microinjection technique.

Role of the blood-cerebrospinal fluid barrier transporter as a cerebral clearance system for prostaglandin E₂ produced in the brain.

An increasing level of prostaglandin (PG) E(2) is involved in the progression of neuroinflammation induced by ischemia and bacterial infection. Although an imbalance in the rates of production and clearance of PGE(2) under these pathological conditions appears to affect the concentration of PGE(2) in the cerebrospinal fluid (CSF), the regulatory system remains incompletely understood. The purpose of this study was to investigate the cellular system of PGE(2) production via microsomal PGE synthetase-1 (mPGES-1), the inducible PGE(2) -generating enzyme, and PGE(2) elimination from the CSF via the blood-CSF barrier (BCSFB).

A clearance system for prostaglandin D2, a sleep-promoting factor, in cerebrospinal fluid: role of the blood-cerebrospinal barrier transporters.

Although the level of prostaglandin (PG) D(2) in cerebrospinal fluid (CSF) affects the action of D-type prostanoid receptors that promote physiological sleep, the regulatory system of PGD(2) clearance from the CSF is not fully understood. The purpose of this study was to investigate PGD(2) elimination from the CSF via the blood-CSF barrier (BCSFB). The in vivo PGD(2) elimination clearance from the CSF was 16-fold greater than that of inulin, which is considered to reflect CSF bulk flow.