PMID- 18945217
OWN - NLM
STAT- MEDLINE
DCOM- 20091109
LR  - 20131121
IS  - 1530-0277 (Electronic)
IS  - 0145-6008 (Linking)
VI  - 33
IP  - 1
DP  - 2009 Jan
TI  - Ethanol attenuates the HFS-induced, ERK-mediated LTP in a dose-dependent manner 
      in rat striatum.
PG  - 121-8
LID - 10.1111/j.1530-0277.2008.00818.x [doi]
AB  - BACKGROUND: The striatum has been implicated to play a role in the control of 
      voluntary behavior, and striatal synaptic plasticity is involved in instrumental 
      learning. Ethanol is known to alter synaptic plasticity, in turn altering the 
      behavior of human and animals. However, it remains unclear whether the striatum 
      plays a role in the effects of ethanol on the central nervous system. The 
      objective of this investigation was to study the effects of acute perfusion of 
      ethanol on long-term potentiation (LTP) to elucidate the mechanisms of addictive 
      drugs in the striatum. In addition, we investigated the contribution of 
      intracellular extracellular signal regulated protein kinase (ERK) signaling 
      pathway to corticostriatal LTP induction. METHODS: The stimulation evoked 
      population spikes (PS) were recorded from the dorsomedial striatum (DMS) slices 
      of rat using the extracellular recording technique. The LTP in DMS slices was 
      induced by high-frequency stimulation (HFS). The ERK level of the DMS was 
      assessed with the Western blot technique. RESULTS: U0126, the inhibitor of ERK, 
      eliminated or significantly attenuated the LTP induced by HFS of the PS in the 
      DMS. MK801 and APV, N-methyl-d-aspartic acid receptor (NMDAR) antagonists, 
      inhibited the induction of striatal LTP, and HFS-induced ERK activation decreased 
      in the slices treated with MK801 in the DMS. Clinically relevant concentrations 
      of ethanol (22 to 88 mM) dose-dependently attenuated the HFS-induced striatal LTP 
      and ERK activation in this brain region. CONCLUSIONS: The LTP of the PS in the 
      DMS is, at least partly, mediated by the ERK pathway coupling to NMDARs. Ethanol 
      attenuated the HFS-induced, ERK-mediated LTP in a dose-dependent manner in this 
      brain region. These results indicate that ethanol may change the synaptic 
      plasticity of corticostriatal circuits underlying the learning of goal-directed 
      instrumental actions, which is mediated by an intracellular ERK signaling pathway 
      associated with NMDARs.
FAU - Xie, Gui Qin
AU  - Xie GQ
AD  - Department of Physiology, Nanjing Medical University, Nanjing, China.
FAU - Wang, Shen Jun
AU  - Wang SJ
FAU - Li, Jing
AU  - Li J
FAU - Cui, Sheng Zhong
AU  - Cui SZ
FAU - Zhou, Rong
AU  - Zhou R
FAU - Chen, Ling
AU  - Chen L
FAU - Yuan, Xiao Ru
AU  - Yuan XR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081018
PL  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (Butadienes)
RN  - 0 (Nitriles)
RN  - 0 (U 0126)
RN  - 3K9958V90M (Ethanol)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Butadienes/pharmacology
MH  - Corpus Striatum/*drug effects/*enzymology
MH  - Dose-Response Relationship, Drug
MH  - Electric Stimulation/methods
MH  - Ethanol/*pharmacology
MH  - Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/*physiology
MH  - Long-Term Potentiation/*drug effects/physiology
MH  - Nitriles/pharmacology
MH  - Organ Culture Techniques
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2008/10/24 09:00
MHDA- 2009/11/10 06:00
CRDT- 2008/10/24 09:00
PHST- 2008/10/24 09:00 [pubmed]
PHST- 2009/11/10 06:00 [medline]
PHST- 2008/10/24 09:00 [entrez]
AID - ACER818 [pii]
AID - 10.1111/j.1530-0277.2008.00818.x [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 2009 Jan;33(1):121-8. doi: 
      10.1111/j.1530-0277.2008.00818.x. Epub 2008 Oct 18.