PMID- 20102565
OWN - NLM
STAT- MEDLINE
DCOM- 20101126
LR  - 20211020
IS  - 1530-0277 (Electronic)
IS  - 0145-6008 (Print)
IS  - 0145-6008 (Linking)
VI  - 34
IP  - 4
DP  - 2010 Apr
TI  - Ethanol acutely inhibits ionotropic glutamate receptor-mediated responses and 
      long-term potentiation in the developing CA1 hippocampus.
PG  - 594-606
LID - 10.1111/j.1530-0277.2009.01128.x [doi]
AB  - BACKGROUND: Developmental ethanol (EtOH) exposure damages the hippocampus, 
      causing long-lasting alterations in learning and memory. Alterations in 
      glutamatergic synaptic transmission and plasticity may play a role in the 
      mechanism of action of EtOH. This signaling is fundamental for synaptogenesis, 
      which occurs during the third trimester of human pregnancy (first 12 days of life 
      in rats). METHODS: Acute coronal brain slices were prepared from 7- to 9-day-old 
      rats. Extracellular and patch-clamp electrophysiological recording techniques 
      were used to characterize the acute effects of EtOH on 
      alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor (AMPAR)- and 
      N-methyl-D-aspartate receptor (NMDAR)-mediated responses and long-term 
      potentiation (LTP) in the CA1 hippocampal region. RESULTS: Ethanol (40 and 80 mM) 
      inhibited AMPAR- and NMDAR-mediated field excitatory postsynaptic potentials 
      (fEPSPs). EtOH (80 mM) also reduced AMPAR-mediated fEPSPs in the presence of an 
      inhibitor of Ca2+ permeable AMPARs. The effect of 80 mM EtOH on NMDAR-mediated 
      fEPSPs was significantly greater in the presence of Mg2+. EtOH (80 mM) neither 
      affected the paired-pulse ratio of AMPAR-mediated fEPSPs nor the presynaptic 
      volley. The paired-pulse ratio of AMPAR-mediated excitatory postsynaptic currents 
      was not affected either, and the amplitude of these currents was inhibited to a 
      lesser extent than that of fEPSPs. EtOH (80 mM) inhibited LTP of AMPAR-mediated 
      fEPSPs. CONCLUSIONS: Acute EtOH exposure during the third-trimester equivalent of 
      human pregnancy inhibits hippocampal glutamatergic transmission and LTP 
      induction, which could alter synapse refinement and ultimately contribute to the 
      pathophysiology of fetal alcohol spectrum disorder.
FAU - Puglia, Michael P
AU  - Puglia MP
AD  - Department of Neurosciences, University of New Mexico Health Sciences Center, 
      Albuquerque, New Mexico 87131-0001, USA.
FAU - Valenzuela, C Fernando
AU  - Valenzuela CF
LA  - eng
GR  - R01-AA15614/AA/NIAAA NIH HHS/United States
GR  - R01 AA015614/AA/NIAAA NIH HHS/United States
GR  - R01 AA015614-05/AA/NIAAA NIH HHS/United States
GR  - T32 AA014127/AA/NIAAA NIH HHS/United States
GR  - F30-AA017813-01/AA/NIAAA NIH HHS/United States
GR  - T32-AA14127/AA/NIAAA NIH HHS/United States
GR  - F30 AA017813/AA/NIAAA NIH HHS/United States
GR  - T32 AA014127-07/AA/NIAAA NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20100126
PL  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Animals
MH  - CA1 Region, Hippocampal/*drug effects/growth & development
MH  - Ethanol/*toxicity
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Female
MH  - Long-Term Potentiation/*drug effects/physiology
MH  - Neural Inhibition/*drug effects/physiology
MH  - Pregnancy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, AMPA/*antagonists & inhibitors/physiology
MH  - Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors/physiology
PMC - PMC3050571
MID - NIHMS272571
EDAT- 2010/01/28 06:00
MHDA- 2010/12/14 06:00
PMCR- 2011/04/01
CRDT- 2010/01/28 06:00
PHST- 2010/01/28 06:00 [entrez]
PHST- 2010/01/28 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
PHST- 2011/04/01 00:00 [pmc-release]
AID - ACER1128 [pii]
AID - 10.1111/j.1530-0277.2009.01128.x [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 2010 Apr;34(4):594-606. doi: 
      10.1111/j.1530-0277.2009.01128.x. Epub 2010 Jan 26.