Abstract

Commentary: Prenatal Ethanol Exposure Persistently Alters Endocannabinoid Signaling and Endocannabinioid-Mediated Excitatory Synaptic Plasticity in Ventral Tegmental Area Dopamine Neurons.

Highlights

  • Medical University of South Carolina, United States David M

  • This reinforcement driving drugseeking behaviors is thought to result from the imbalance in glutamate homeostasis that disrupts the mesocorticolimbic dopamine (DA) pathways (Kalivas, 2009)

  • Positive Reinforcement in Drug Addiction by chronic ethanol administration (Basavarajappa and Hungund, 1999; Xia et al, 2006; Mitrirattanakul et al, 2007; DePoy et al, 2013; Varodayan et al, 2016). eCB-long-term depression (LTD) in midbrain DA neurons was mediated by reduced presynaptic glutamate release (HajDahmane and Shen, 2010)

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Summary

Introduction

Medical University of South Carolina, United States David M. Prenatal Ethanol Exposure Persistently Alters Endocannabinoid Signaling and Endocannabinoid-Mediated Excitatory Synaptic Plasticity in Ventral Tegmental Area Dopamine Neurons by Hausknecht, K., Shen, Y.-L., Wang, R.-X., Haj-Dahmane, S., and Shen R.-Y. Expanding this line of research, a recent work (Hausknecht et al, 2017) discovered that PE exposure persistently impaired eCB long-term depression (LTD) at excitatory synapses in rats.

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