BPB Reports
Online ISSN : 2434-432X
Huperzia serrata and the Constitute of Huperzine A Attenuate MK-801-Induced Cognitive Dysfunction in Mice via PKC-Erk Pathway
Takuya OhbaHonoka FujimoriShinsuke NakamuraYoshihiro HayashiHiroyuki KonoMasamitsu ShimazawaHideaki Hara
Author information

2021 Volume 4 Issue 5 Pages 155-161


N-methyl-D-aspartate (NMDA) receptor has important role in synapse function and neurotransmission by the high permeability of Ca2+. In Alzheimer’s disease (AD), NMDA mediated neurotransmission is impaired by decreasing NMDA receptor subunits and increasing glutamate, which is an NMDA receptor ligand. Therefore, the NMDA antagonist (memantine) is used as a therapeutic drug of AD. Huperzia serrata is a traditional Chinese herbal medicine, and the constitute huperzine A has been reported to inhibit NMDA receptor. In this study, we clarified the effect of Huperzia serrata and the constitute huperzine A on MK-801-induced cognitive dysfunction. Memantine, Huperzia serrata and huperzine A were administered orally once a day and Y-maze test was performed at day 7 to investigate cognitive function. After Y-maze test, mice brains were collected and evaluated the expression levels of glutamate receptors and Ca2+ signalling associated protein. Memantine (5 mg/kg, p.o.), Huperzia serrata (1000 mg/kg, p.o.) and huperzine A (0.7 mg/kg, p.o.) were improved collect alternation behaviour in Y-maze test. Treatment of memantine, Huperzia serrata and huperzine A also improved the total arm entries increased by MK-801. The expression level of NMDA receptor subunit NR2A was increased by Huperzia serrata and huperzine A treatment. In addition, the decreased expression level of PKCα and phosphorylation of Erk1/2 by MK-801 were improved. These results suggest that Huperzia serrata and the constitute huperzine A improve cognitive dysfunction through NMDA receptor function and glutaminergic signaling pathway.

Information related to the author
© 2021 The Pharmaceutical Society of Japan

BPB Reports applies the Creative Commons Attribution (CCBY) license to works we published. The license was developed to facilitate open access - namely, free immediate access to, and unrestricted reuse of, original works to all types. Under this license, authors agree to make articles legally available for reuse, without permissions of fees, for virtually any purpose. Anyone may copy, distribute, or reuse these articles, as long as the author and original source are properly cited.
Previous article Next article