Differential binding of CREB and REST/NRSF to NMDAR1 promoter is associated with the sex-selective cognitive deficit following postnatal PBDE-209 exposure in mice.

Neonatal exposure to decabromodiphenyl ether (PBDE-209), a widely used flame retardant, affects cognitive performances in the later stage of life in a sex-dependent manner. PBDE-209 interferes with glutamatergic signaling and N-methyl-D-aspartate receptor (NMDAR) subunits with unresolved regulatory mechanisms. This study exposed male and female mice pups through postnatal day (PND) 3-10 to PBDE-209 (oral dose: 0, 6, or 20 mg/kg body weight).

CDRI-08 Attenuates REST/NRSF-Mediated Expression of NMDAR1 Gene in PBDE-209-Exposed Mice Brain.

CDRI-08 is a standardized bacoside enriched ethanolic extract of Bacopa monnieri, a nootropic plant. We reported that CDRI-08 attenuated oxidative stress and memory impairment in mice, induced by a flame retardant, PBDE-209. In order to explore the mechanism, present study was designed to examine the role of CDRI-08 on the expression of NMDAR1 (NR1) and the binding of REST/NRSF to NR1 promoter against postnatal exposure of PBDE-209.

Neuromodulatory role of Bacopa monnieri on oxidative stress induced by postnatal exposure to decabromodiphenyl ether (PBDE -209) in neonate and young female mice.

Objectives: Bacopa monnieri (BM), a traditional ayurvedic medicine, is a well-known memory enhancer. We have explored the role of BM against decabrominated diphenyl ether (PBDE-209)-induced alterations in neonate and young female mice.

Materials And Methods: Mice were orally administered with B.