Parishin C's prevention of Aβ 1-42-induced inhibition of long-term potentiation is related to NMDA receptors.
10.1016/j.apsb.2016.03.009
- Author:
Zhihui LIU
1
;
Weiping WANG
1
;
Nan FENG
1
;
Ling WANG
1
;
Jiangong SHI
1
;
Xiaoliang WANG
1
Author Information
1. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
- Publication Type:Journal Article
- Keywords:
Ion channels;
Long-term potentiation;
NMDA receptors;
Neuroprotection;
Parishin C
- From:
Acta Pharmaceutica Sinica B
2016;6(3):189-197
- CountryChina
- Language:English
-
Abstract:
The rhizome of Gastrodia elata (GE), a herb medicine, has been used for treatment of neuronal disorders in Eastern Asia for hundreds of years. Parishin C is a major ingredient of GE. In this study, the i.c.v. injection of soluble Aβ 1-42 oligomers model of LTP injury was used. We investigated the effects of parishin C on the improvement of LTP in soluble Aβ 1-42 oligomer-injected rats and the underlying electrophysiological mechanisms. Parishin C (i.p. or i.c.v.) significantly ameliorated LTP impairment induced by i.c.v. injection of soluble Aβ 1-42 oligomers. In cultured hippocampal neurons, soluble Aβ 1-42 oligomers significantly inhibited NMDAR currents while not affecting AMPAR currents and voltage-dependent currents. Pretreatment with parishin C protected NMDA receptor currents from the damage induced by Aβ. In summary, parishin C improved LTP deficits induced by soluble Aβ 1-42 oligomers. The protection by parishin C against Aβ-induced LTP damage might be related to NMDA receptors.
