Liuwei Dihuang decoction facilitates the induction of long-term potentiation (LTP) in senescence accelerated mouse/prone 8 (SAMP8) hippocampal slices by inhibiting voltage-dependent calcium channels (VDCCs) and promoting N-methyl-d-aspartate receptor (NMDA) receptors.
BACKGROUND
Liuwei Dihuang decoction (LW) is a typical traditional Chinese medicine (TCM) prescription and consists of six herbs including Rehmannia glutinosa Libosch. (family: Scrophulariaceae), Cornus officinalis Sieb. (family: Cornaceae), Dioscorea opposite Thunb. (family: Dioscoreaceae), Alisma orientale (G. Samuelsson) Juz (family: Alismataceae), Poria cocos (Schw.)Wolf (family: Polyporaceae) and Paeonia suffruticosa Andrews (family: Paeoniaceae). It has long been used clinically in treatment of many kinds of diseases with the sign of Yin insufficiency of kidney.


OBJECTIVE
Our previous pharmacological studies demonstrated that LW possesses effect of ameliorating the decline of the learning and memory in senescence accelerated mouse/prone 8 (SAMP8), but the mechanism has not been well established. LW-containing serum (LWCS) is used in the current study to elucidate the possible mechanisms.


METHODS
6-month-old SAMP8 was used in this study to investigate the effect of LWCS on the induction of long-term potentiation (LTP). Primary cultured hippocampal neurons were used in this study to investigate the effects of LWCS on [Ca(2+)](i), I(Ca) and N-Methyl-d-aspartate (NMDA)-evoked currents. [Ca(2+)](i) was imaged using Fluo-3 and whole-cell patch recordings were applied to study the I(Ca) and NMDA-evoked currents.


RESULTS
We find that LWCS facilitates the induction of LTP in hippocampal slices of 6-month-old SAMP8. In primary cultured hippocampal neurons, LWCS increases intracellular [Ca(2+)](i), the I(Ca) is suppressed by LWCS, and NMDA-evoked currents are promoted.


CONCLUSIONS
These results indicate that LW improves the synaptic plasticity by inhibiting voltage-dependent calciumchannels (VDCCs) and promoting the function of NMDA receptors. This improvement might be one of the mechanisms contributing to cognitive improvement effect of LW.
Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China.
Yan
Y
Huang
Heping
H
Zhang
Sheng
S
Yang
Haifa
H
Qiao
Wenxia
W
Zhou
Yongxiang
Y
Zhang
D019588:Aging, Premature; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D003071:Cognition / Q000187:drug effects; D004365:Drugs, Chinese Herbal / Q000494:pharmacology* / Q000627:therapeutic use; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D007668:Kidney; D007858:Learning; D017774:Long-Term Potentiation / Q000187:drug effects*; D019684:Magnoliopsida; D008297:Male; D008568:Memory / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D008517:Phytotherapy; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D016710:Yin Deficiency
D015220:Calcium Channels; D004365:Drugs, Chinese Herbal; C042579:Liuwei Dihuang Decoction; D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium