Poria cocos ethanol extract and its active constituent, pachymic acid, modulate sleep architectures via activation of GABA(A)-ergic transmission in rats.
10.12729/jbr.2015.16.3.084
- Author:
Vikash Kumar SHAH
1
;
Sam Shik NA
;
Myong Soo CHONG
;
Jae Hoon WOO
;
Yeong Ok KWON
;
Mi Kyeong LEE
;
Ki Wan OH
Author Information
1. College of Pharmacy and Medical Research Center (MRC), Chungbuk National University, Cheongju 28644, Korea. kiwan@chungbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Poria cocos ethanol extract;
Pachymic acid;
Non-rapid eye movement sleep;
Cl- influx;
glutamic acid decarboxylase;
GABA(A)-ergic systems
- MeSH:
Administration, Oral;
Animals;
Asian Continental Ancestry Group;
China;
Cocos*;
Electroencephalography;
Ethanol*;
Eye Movements;
Glutamate Decarboxylase;
Humans;
Japan;
Korea;
Medicine, Chinese Traditional;
Neurons;
North America;
Pinus;
Poria*;
Rats*;
Receptors, GABA-A;
Sleep Initiation and Maintenance Disorders
- From:Journal of Biomedical Research
2015;16(3):84-92
- CountryRepublic of Korea
- Language:English
-
Abstract:
Poria cocos is a well-known traditional Chinese traditional medicine (TCM) that grows around roots of pine trees in China, Korea, Japan, and North America. Poria cocos has been used in Asian countries to treat insomnia as either a single herb or part of an herbal formula. In a previous experiment, pachymic acid (PA), an active constituent of Poria cocos ethanol extract (PCE), increased pentobarbital-induced sleeping behaviors. The aim of this experiment was to evaluate whether or not PCE and PA modulate sleep architectures in rats as well as whether or not their effects are mediated through GABA(A)-ergic transmission. PCE and PA were orally administered to individual rats 7 days after surgical implantation of a transmitter, and sleep architectures were recorded by Telemetric Cortical encephalogram (EEG) upon oral administration of test drugs. PCE and PA increased total sleep time and non-rapid eye movement (NREM) sleep as well as reduced numbers of sleep/wake cycles recorded by EEG. Furthermore, PCE increased intracellular chloride levels, GAD65/67 protein levels, and alpha-, beta-, and gamma-subunits of GABA(A) receptors in primary cultured hypothalamic neuronal cells. These data suggest that PCE modulates sleep architectures via activation of GABA(A)-ergic systems. Further, as PA is an active component of PCE, they may have the same pharmacological effects.
