Gestational nicotine exposure reduces nicotinic cholinergic receptor (nAChR) expression in dopaminergic brain regions of adolescent rats

Hao Chen, Steven L. Parker, Shannon G. Matta, Burt Sharp

Research output: Contribution to journalArticle

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Abstract

Children of women who smoked during pregnancy are at increased risk of dependence when smoking is initiated during adolescence. We previously reported that gestational nicotine exposure attenuated dopamine release induced by nicotine delivered during adolescence. In this study, we determined the effects of gestational nicotine exposure on nicotinic cholinergic receptor (nAChR) expression. Timed pregnant rats received nicotine (2 mg/kg/day) or vehicle via mini-osmotic pumps during gestation. Treatments continued in pups via maternal nursing during postnatal days (PN) 2-14 (equivalent to the human in utero third trimester). On PN35, 125l-epibatidine binding to nAChR was measured. The Bmax values (fmol/mg) in prefrontal cortex (PFC), nucleus accumbens (NAcc), substantia nigra (SN) and ventral tegmental area (VTA) were reduced by 26.6% (P < 0.05), 32.6% (P < 0.01), 23.0% (P < 0.01) and 27.6% (P < 0.05), respectively. In addition, gender differences were found in vehicle-treated groups; in SN and VTA, females were 79.3% (P < 0.005) and 82.9% (P = 0.08) of males, respectively. The expression of nAChR subunit mRNAs was measured using real-time RT-PCR on laser-capture microdissected tissues. In adolescent VTA, gestational nicotine exposure reduced (P < 0.05) nAChR subunit mRNAs encoding α3 (53.0%), α4 (23.9%), α5 (46.7%) and 4 (61.4%). In NAcc core, the treatment increased α3 mRNA (75.8%). In addition, the number of neurons in VTA was reduced by 15.0% (P < 0.001). These studies indicate that gestational exposure to nicotine induces long-lasting changes in nAChR expression that may underlie the vulnerability of adolescents to dependence on nicotine.

Original languageEnglish (US)
Pages (from-to)380-388
Number of pages9
JournalEuropean Journal of Neuroscience
Volume22
Issue number2
DOIs
StatePublished - Jul 1 2005

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Nicotinic Receptors
Cholinergic Receptors
Nicotine
Ventral Tegmental Area
Brain
epibatidine
Nucleus Accumbens
Substantia Nigra
Messenger RNA
Pregnancy
Tobacco Use Disorder
Third Pregnancy Trimester
Prefrontal Cortex
Real-Time Polymerase Chain Reaction
Dopamine
Lasers
Nursing
Smoking
Mothers
Neurons

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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Gestational nicotine exposure reduces nicotinic cholinergic receptor (nAChR) expression in dopaminergic brain regions of adolescent rats. / Chen, Hao; Parker, Steven L.; Matta, Shannon G.; Sharp, Burt.

In: European Journal of Neuroscience, Vol. 22, No. 2, 01.07.2005, p. 380-388.

Research output: Contribution to journalArticle

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abstract = "Children of women who smoked during pregnancy are at increased risk of dependence when smoking is initiated during adolescence. We previously reported that gestational nicotine exposure attenuated dopamine release induced by nicotine delivered during adolescence. In this study, we determined the effects of gestational nicotine exposure on nicotinic cholinergic receptor (nAChR) expression. Timed pregnant rats received nicotine (2 mg/kg/day) or vehicle via mini-osmotic pumps during gestation. Treatments continued in pups via maternal nursing during postnatal days (PN) 2-14 (equivalent to the human in utero third trimester). On PN35, 125l-epibatidine binding to nAChR was measured. The Bmax values (fmol/mg) in prefrontal cortex (PFC), nucleus accumbens (NAcc), substantia nigra (SN) and ventral tegmental area (VTA) were reduced by 26.6{\%} (P < 0.05), 32.6{\%} (P < 0.01), 23.0{\%} (P < 0.01) and 27.6{\%} (P < 0.05), respectively. In addition, gender differences were found in vehicle-treated groups; in SN and VTA, females were 79.3{\%} (P < 0.005) and 82.9{\%} (P = 0.08) of males, respectively. The expression of nAChR subunit mRNAs was measured using real-time RT-PCR on laser-capture microdissected tissues. In adolescent VTA, gestational nicotine exposure reduced (P < 0.05) nAChR subunit mRNAs encoding α3 (53.0{\%}), α4 (23.9{\%}), α5 (46.7{\%}) and 4 (61.4{\%}). In NAcc core, the treatment increased α3 mRNA (75.8{\%}). In addition, the number of neurons in VTA was reduced by 15.0{\%} (P < 0.001). These studies indicate that gestational exposure to nicotine induces long-lasting changes in nAChR expression that may underlie the vulnerability of adolescents to dependence on nicotine.",
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