Prenatal stress induces vulnerability to nicotine addiction and alters D2 receptors' expression in the nucleus accumbens in adult rats

Neuroscience. 2015 Sep 24:304:279-85. doi: 10.1016/j.neuroscience.2015.07.029. Epub 2015 Jul 17.

Abstract

Prenatal stress (PS) can induce several long-lasting behavioral and molecular abnormalities in rats. It can also be considered as a risk factor for many psychiatric diseases like schizophrenia, depression or PTSD and predispose to addiction. In this study, we investigated the effect of prenatal stress on the reinforcing properties of nicotine in the CPP paradigm. Then, we examined the mRNA expression of the D2 dopaminergic receptors using the quantitative real-time PCR technique in the nucleus accumbens (NAcc). We found that prenatally stressed rats exhibited a greater place preference for the nicotine-paired compartment than the control rats. Moreover, we observed an overexpression of the DRD2 gene in adult offspring stressed in utero and a downregulation in the PS NIC group (PS rats treated with nicotine) compared with their control counterparts (C NIC). These data suggest that maternal stress can permanently alter the offspring's addictive behavior and D2 receptors' expression.

Keywords: DRD2 mRNA expression; conditioned place preference; nicotine; nucleus accumbens; prenatal stress; qPCR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Conditioning, Psychological / drug effects
  • Conditioning, Psychological / physiology
  • Disease Models, Animal
  • Female
  • Male
  • Nicotine / administration & dosage
  • Nicotinic Agonists / administration & dosage
  • Nucleus Accumbens / drug effects
  • Nucleus Accumbens / growth & development
  • Nucleus Accumbens / metabolism*
  • Polymerase Chain Reaction
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • RNA, Messenger / metabolism
  • Rats, Wistar
  • Receptors, Dopamine D2 / metabolism*
  • Spatial Behavior / drug effects
  • Spatial Behavior / physiology
  • Stress, Psychological / physiopathology*
  • Tobacco Use Disorder / physiopathology*

Substances

  • DRD2 protein, rat
  • Nicotinic Agonists
  • RNA, Messenger
  • Receptors, Dopamine D2
  • Nicotine