PMID- 19118821
OWN - NLM
STAT- MEDLINE
DCOM- 20090519
LR  - 20211020
IS  - 1873-2402 (Electronic)
IS  - 0006-3223 (Print)
IS  - 0006-3223 (Linking)
VI  - 65
IP  - 8
DP  - 2009 Apr 15
TI  - Strain specific synaptic modifications on ventral tegmental area dopamine neurons 
      after ethanol exposure.
PG  - 646-53
LID - 10.1016/j.biopsych.2008.10.042 [doi]
AB  - BACKGROUND: Genetic factors and previous alcohol experience influence alcohol 
      consumption in both humans and rodents. Specifically, a prior experience with 
      ethanol increases ethanol intake in both ethanol-preferring C57BL/6 (C57) and 
      ethanol non-preferring DBA/2 (DBA) mice. Whereas the ventral tegmental area (VTA) 
      importantly regulates dopamine levels and ethanol intake, it is unknown whether 
      ethanol experience differentially alters synaptic properties of VTA dopamine 
      neurons in ethanol-preferring and non-preferring mice. METHODS: The properties of 
      excitatory and inhibitory inputs and the ability to elicit long-term potentiation 
      (LTP) were assessed with whole-cell patch-clamp recordings in VTA dopamine 
      neurons from C57 and DBA mice 24 hours after a single ethanol (2 g/kg, IP) or 
      equivalent saline injection. RESULTS: Ethanol exposure increased 
      gamma-aminobutyric acid (GABA) release onto VTA dopamine neurons in DBA mice, as 
      previously observed in C57 mice. However, a single ethanol exposure reduced 
      alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and 
      N-methyl-D-aspartate receptor (NMDAR) function and LTP in VTA dopamine neurons 
      from DBA but not C57 mice. CONCLUSIONS: A single ethanol exposure selectively 
      reduced glutamate receptor function in VTA dopamine neurons from the ethanol 
      non-preferring DBA strain but enhanced GABA signaling in both C57 and DBA 
      strains. These results support the notion that VTA dopamine neurons are a central 
      target of ethanol-induced neural plasticity, which could contribute to ethanol 
      consumption. Furthermore, these findings highlight the possible need for 
      specialized therapeutic interventions for alcoholism based on individual 
      intrinsic differences.
FAU - Wanat, Matthew J
AU  - Wanat MJ
AD  - Neuroscience Graduate Program, University of California-San Francisco, San 
      Francisco, California, USA.
FAU - Sparta, Dennis R
AU  - Sparta DR
FAU - Hopf, F Woodward
AU  - Hopf FW
FAU - Bowers, M Scott
AU  - Bowers MS
FAU - Melis, Miriam
AU  - Melis M
FAU - Bonci, Antonello
AU  - Bonci A
LA  - eng
GR  - F31 DA21464-01/DA/NIDA NIH HHS/United States
GR  - R01 DA016782/DA/NIDA NIH HHS/United States
GR  - R01 DA016782-04/DA/NIDA NIH HHS/United States
GR  - T32 AA009455/AA/NIAAA NIH HHS/United States
GR  - F31 DA021464-03/DA/NIDA NIH HHS/United States
GR  - R01 DA016782-05A1/DA/NIDA NIH HHS/United States
GR  - F31 DA021464/DA/NIDA NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20081231
PL  - United States
TA  - Biol Psychiatry
JT  - Biological psychiatry
JID - 0213264
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3K9958V90M (Ethanol)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Dopamine/*metabolism
MH  - Ethanol/*pharmacology
MH  - In Vitro Techniques
MH  - Long-Term Potentiation/drug effects
MH  - Mice
MH  - Mice, Inbred C57BL/metabolism/*physiology
MH  - Mice, Inbred DBA/metabolism/*physiology
MH  - Neuronal Plasticity/*drug effects
MH  - Neurons/metabolism
MH  - Presynaptic Terminals/*drug effects/physiology
MH  - Receptors, AMPA/antagonists & inhibitors
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
MH  - Species Specificity
MH  - Ventral Tegmental Area/*drug effects/metabolism/*physiology
MH  - gamma-Aminobutyric Acid/metabolism
PMC - PMC3040034
MID - NIHMS219946
EDAT- 2009/01/03 09:00
MHDA- 2009/05/20 09:00
PMCR- 2011/02/16
CRDT- 2009/01/03 09:00
PHST- 2007/12/17 00:00 [received]
PHST- 2008/10/29 00:00 [revised]
PHST- 2008/10/30 00:00 [accepted]
PHST- 2009/01/03 09:00 [entrez]
PHST- 2009/01/03 09:00 [pubmed]
PHST- 2009/05/20 09:00 [medline]
PHST- 2011/02/16 00:00 [pmc-release]
AID - S0006-3223(08)01391-7 [pii]
AID - 10.1016/j.biopsych.2008.10.042 [doi]
PST - ppublish
SO  - Biol Psychiatry. 2009 Apr 15;65(8):646-53. doi: 10.1016/j.biopsych.2008.10.042. 
      Epub 2008 Dec 31.