Background—
The posterior ventral tegmental area (pVTA) mediates the reinforcing and
stimulating effects of ethanol (EtOH). Electrophysiological studies indicated that exposure to
EtOH increased glutamate synaptic function in the VTA. The current study determined the
neurochemical effects of both acute and repeated EtOH exposure on glutamate neurotransmission
in the pVTA.
Methods—
Adult female Wistar rats were implanted with microdialysis probes in the pVTA.
During microdialysis, rats received acute i.p. injection of saline or EtOH (0.5, 1.0 or 2.0 g/kg) and
extracellular glutamate levels were measured in the pVTA. The effects of repeated daily injections
of EtOH (0.5, 1.0, or 2.0 g/kg) on basal extracellular glutamate concentrations in the pVTA and on
glutamate response to a subsequent EtOH challenge were also examined.
Results—
The injection of 0.5 g/kg EtOH significantly increased (120–125 % of baseline),
whereas injection of 2.0 g/kg EtOH significantly decreased (80% of baseline) extracellular
glutamate levels in the pVTA. The dose of 1.0 g/kg EtOH did not alter extracellular glutamate
levels. Seven repeated daily injections of each dose of EtOH increased basal extracellular
glutamate concentrations (from 4.1 ± 0.5 to 9.2 ± 0.5 μM) and reduced glutamate clearance in the
pVTA (from 30 ± 2% to 17 ± 2%), but failed to alter glutamate response to a 2.0 g/kg EtOH
challenge.
Conclusion—
The results suggest that the low dose of EtOH can stimulate the release of
glutamate in the pVTA, and repeated EtOH administration increased basal glutamate transmission
in the pVTA, as a result of reduced glutamate clearance
