Hydrophilic compartments of Capsosiphon fulvescens protein alleviate impaired spatial memory by regulating BDNF-mediated ER stress against chronic ethanol exposure

- Cf-CP administration for 14 days upregulated mBDNF expression in the hippocampus.
- Spatial memory was enhanced by Cf-CP until withdrawal 35 days.
- Increase of mBDNF by Cf-CP was maintained until withdrawal 35 days.
- Impairment of spatial memory by chronic ethanol was reduced by Cf-CP co-treat.
- Cf-CP downregulated GRP78 expression and PKC phosphorylation by the ethanol exposure.

Seaweed-derived antioxidative proteins can protect brain against ethanol-induced oxidative stress. This study was to investigate whether Capsosiphon fulvescens crude proteins (Cf-CP) alleviates the impairment in spatial memory by regulating brain-derived neurotrophic factor (BDNF) and endoplasmic reticulum (ER) stress against chronic ethanol exposure. Oral administration of Cf-CP for 14 consecutive days increased mature BDNF (mBDNF) levels and phosphorylation of calcium/calmodulin-dependent protein kinase II in rat dorsal hippocampus. The latency to platform was decreased and an increase in mBDNF was maintained until the withdrawal at 35 days in Cf-CP treatment. In rats treated with ethanol for four weeks, the ethanol-induced impairment in spatial memory was reduced by co-administration of Cf-CP. This treatment prevented the decrease in mBDNF and the increase in both of ER stress response protein, glucose-regulated protein 78, and protein kinase C delta phosphorylation. These findings suggest that Cf-CP administration improve cognitive functions by regulating BDNF-mediated ER stress response in the dorsal hippocampus.