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Strain specific synaptic modifications on ventral tegmental area dopamine neurons after ethanol exposure
Matthew J Wanat1, Dennis R Sparta, F Woodward Hopf
1Neuroscience Graduate Program, University of California-San Francisco, San Francisco, California, USA.
Biological Psychiatry
|January 3, 2009
Summary
Ethanol exposure alters brain plasticity differently in mice preferring alcohol versus those that do not. Non-preferring mice showed reduced glutamate receptor function in ventral tegmental area dopamine neurons, while both strains had increased GABA signaling.
Area of Science:
- Neuroscience
- Addiction Research
- Pharmacology
Background:
- Alcohol consumption is influenced by genetics and prior alcohol experience.
- Ethanol intake increases after previous exposure in both ethanol-preferring (C57BL/6) and non-preferring (DBA/2) mice.
- The ventral tegmental area (VTA) regulates dopamine and alcohol intake, but its dopamine neurons' synaptic plasticity post-ethanol exposure is not fully understood across different genetic strains.
Purpose of the Study:
- To investigate how a single ethanol exposure differentially affects synaptic properties of VTA dopamine neurons in ethanol-preferring (C57) and non-preferring (DBA) mice.
- To determine if ethanol experience alters excitatory and inhibitory inputs and long-term potentiation (LTP) in VTA dopamine neurons.
- To explore the role of VTA dopamine neurons in ethanol-induced neural plasticity and consumption.
Main Methods:
- Whole-cell patch-clamp recordings were used to assess synaptic properties in VTA dopamine neurons.
- Experiments were conducted on C57 and DBA mice 24 hours after a single injection of ethanol or saline.
- Evaluated excitatory and inhibitory inputs, and the capacity for long-term potentiation (LTP).
Main Results:
- Ethanol exposure increased gamma-aminobutyric acid (GABA) release onto VTA dopamine neurons in both DBA and C57 mice.
- A single ethanol exposure reduced alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and N-methyl-D-aspartate receptor (NMDAR) function in DBA mice, but not C57 mice.
- Long-term potentiation (LTP) was reduced in VTA dopamine neurons of DBA mice following ethanol exposure, but not in C57 mice.
Conclusions:
- Ethanol exposure selectively impairs glutamate receptor function in VTA dopamine neurons of ethanol non-preferring mice (DBA).
- Ethanol enhances GABA signaling in VTA dopamine neurons of both ethanol-preferring (C57) and non-preferring (DBA) mice.
- These findings suggest VTA dopamine neurons are key targets for ethanol-induced plasticity, potentially influencing alcohol consumption and highlighting the need for personalized alcoholism treatments.
