Inhibition of prolactin with bromocriptine for 28 days increases blood–brain barrier permeability in the rat. (20th August 2015)

• Record Type: Journal Article
• Authors: Rosas-Hernandez, H.; Ramirez, M.; Ramirez-Lee, M.A.; Ali, S.F.; Gonzalez, C.
• Is Part Of: Neuroscience. Volume 301(2015)
• Page Start: 61
• Page End: 70
• Publication Date: 2015-08-20
• Subjects: AF amniotic fluid -- BBB blood–brain barrier -- bBMVECs bovine brain microvessel endothelial cells -- Bromo bromocriptine -- DMF N, N-dimethylformamide -- EB Evans Blue -- FITC fluorescein isothiocyanate -- GFAP glial fibrillary acidic protein -- GH growth hormone -- HRP horseradish peroxidase -- LPS lipopolysaccharide -- Meth methamphetamine -- PRL prolactin -- PRLR PRL receptor -- TEER trans endothelial electrical resistance -- TJs tight junctions -- VEGF vascular endothelial growth factor; prolactin -- blood–brain barrier -- lipopolysaccharide -- tight junctions -- permeability; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2015.05.066
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: 28 days Bromo treatment inhibited PRL synthesis. 28 days Bromo treatment increased BBB permeability and induced edema formation. 28 days Bromo treatment decreased the expression of claudin-5 and occludin. 28 days Bromo treatment potentiated LPS-induced damage to the BBB. Abstract: The blood–brain barrier (BBB) is necessary for the proper function of the brain. Its maintenance is regulated by endogenous factors. Recent evidences suggest prolactin (PRL) regulates the BBB properties in vitro, nevertheless no evidence of these effects have been reported in vivo . The aim of this study was to evaluate the role of PRL in the maintenance of the BBB in the rat. Male Wistar rats were treated with Bromocriptine (Bromo) to inhibit PRL production for 28 days in the absence or presence of lipopolysaccharide (LPS). BBB permeability was evaluated through the Evans Blue dye and fluorescein-dextran extravasation as well as through edema formation. The expression of claudin-5, occludin, glial fibrillary acidic protein (GFAP) and the PRL receptor (PRLR) was evaluated through western blot. Bromo reduced the physiological levels of PRL at 28 days. At the same time, Bromo increased BBB permeability and edema formation associated with a decrement in claudin-5 and occludin and potentiated the increase in BBB permeability induced by LPS. However, no neuroinflammation was detected, since the expression of GFAP was unchanged, as well as the expression of the PRLR. These data provide the first evidence that inhibition of PRL with Bromo affects the maintenance of the BBB through modulating the expression of tight junction proteins in vivo.