Ethanol Increases Glutamate Neurotransmission in the Posterior Ventral Tegmental Area of Female Wistar Rats

Zheng Ming Ding, Eric Engleman, Zachary Rodd, William J. Mcbride

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

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. This 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 intraperitoneal (i.p.) injection of saline or EtOH (0.5, 1.0, or 2.0g/kg), and extracellular glutamate levels were measured in the pVTA. The effects of repeated daily injections of EtOH (0.5, 1.0, or 2.0g/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 0.5g/kg EtOH significantly increased (120 to 125% of baseline), whereas injection of 2.0g/kg EtOH significantly decreased (80% of baseline) extracellular glutamate levels in the pVTA. The dose of 1.0g/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±0.5μM) and reduced glutamate clearance in the pVTA (from 30±2 to 17±2%), but failed to alter glutamate response to a 2.0g/kg EtOH challenge. Conclusions: 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.

Original languageEnglish
Pages (from-to)633-640
Number of pages8
JournalAlcoholism: Clinical and Experimental Research
Volume36
Issue number4
DOIs
StatePublished - Apr 2012

Fingerprint

Ventral Tegmental Area
Synaptic Transmission
Wistar Rats
Rats
Glutamic Acid
Ethanol
Injections
Microdialysis
Intraperitoneal Injections

Keywords

  • Ethanol
  • Glutamate
  • Microdialysis
  • Ventral Tegmental Area

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Psychiatry and Mental health
  • Toxicology

Cite this

Ethanol Increases Glutamate Neurotransmission in the Posterior Ventral Tegmental Area of Female Wistar Rats. / Ding, Zheng Ming; Engleman, Eric; Rodd, Zachary; Mcbride, William J.

In: Alcoholism: Clinical and Experimental Research, Vol. 36, No. 4, 04.2012, p. 633-640.

Research output: Contribution to journalArticle

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abstract = "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. This 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 intraperitoneal (i.p.) injection of saline or EtOH (0.5, 1.0, or 2.0g/kg), and extracellular glutamate levels were measured in the pVTA. The effects of repeated daily injections of EtOH (0.5, 1.0, or 2.0g/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 0.5g/kg EtOH significantly increased (120 to 125{\%} of baseline), whereas injection of 2.0g/kg EtOH significantly decreased (80{\%} of baseline) extracellular glutamate levels in the pVTA. The dose of 1.0g/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±0.5μM) and reduced glutamate clearance in the pVTA (from 30±2 to 17±2{\%}), but failed to alter glutamate response to a 2.0g/kg EtOH challenge. Conclusions: 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.",
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N2 - 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. This 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 intraperitoneal (i.p.) injection of saline or EtOH (0.5, 1.0, or 2.0g/kg), and extracellular glutamate levels were measured in the pVTA. The effects of repeated daily injections of EtOH (0.5, 1.0, or 2.0g/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 0.5g/kg EtOH significantly increased (120 to 125% of baseline), whereas injection of 2.0g/kg EtOH significantly decreased (80% of baseline) extracellular glutamate levels in the pVTA. The dose of 1.0g/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±0.5μM) and reduced glutamate clearance in the pVTA (from 30±2 to 17±2%), but failed to alter glutamate response to a 2.0g/kg EtOH challenge. Conclusions: 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.

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