Late emerging effects of prenatal and early postnatal nicotine exposure on the cholinergic system and anxiety-like behavior

Eppolito, Amy K.; Bachus, Susan E.; McDonald, Craig G.; Meador‐Woodruff, James H.; Smith, Robert F.

doi:10.1016/j.ntt.2009.12.009

Cited by 62 publications

(51 citation statements)

References 42 publications

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“…The deficits in basal synaptic transmission and LTP could be associated with alterations in nAChR subtypes that lend a modulatory role synaptic transmission and plasticity [75,76]. This notion is supported by a recent finding that mRNA levels of a7-nAChRs were reduced in the hippocampus of rats exposed to nicotine prenatally [20]. In summary, these findings strongly suggest that prenatal nicotine exposure results in potent glutamatergic impairment in the excitatory transmission in the hippocampus.…”

Section: Discussionmentioning

confidence: 55%

“…In a previous report, we demonstrated that in 2-month-old rats prenatally exposed to nicotine, the AMPA receptor-mediated synaptic currents were significantly reduced, suggesting long-lasting impairment in excitatory synaptic physiology [17]. Importantly, disruptions in the hippocampal glutamatergic system are attributed to mood disorders like anxiety and depression [18,19] and several animal studies provided accounts on neurobehavioral outcomes of prenatal nicotine exposure [17,20,21]. However, there is a lack of understanding of the possible molecular mechanisms contributing to these behavioral outcomes and if they are specifically related to hippocampus and its major excitatory neurotransmitter system.…”

Section: Introductionmentioning

confidence: 92%

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Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus

Parameshwaran

Buabeid

Karuppagounder

et al. 2011

Cell. Mol. Life Sci.

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In the developing brain, nicotinic acetylcholine receptors (nAChRs) are involved in cell survival, targeting, formation of neural and sensory circuits, and development and maturation of other neurotransmitter systems. This regulatory role is disrupted when the developing brain is exposed to nicotine, which occurs with tobacco use during pregnancy. Prenatal nicotine exposure has been shown to be a strong risk factor for memory deficits and other behavioral aberrations in the offspring. The molecular mechanisms underlying these neurobehavioral outcomes are not clearly elucidated. We used a rodent model to assess behavioral, neurophysiological, and neurochemical consequences of prenatal nicotine exposure in rat offspring with specific emphasis on the hippocampal glutamatergic system. Pregnant dams were infused with nicotine (6 mg/kg/day) subcutaneously from the third day of pregnancy until birth. Results indicate that prenatal nicotine exposure leads to increased anxiety and depressive-like effects and impaired spatial memory. Synaptic plasticity in the form of long-term potentiation (LTP), basal synaptic transmission, and AMPA receptor-mediated synaptic currents were reduced. The deficit in synaptic plasticity was paralleled by declines in protein levels of vesicular glutamate transporter 1 (VGLUT1), synaptophysin, AMPA receptor subunit GluR1, phospho(Ser845) GluR1, and postsynaptic density 95 (PSD-95). These results suggest that prenatal nicotine exposure by maternal smoking could result in alterations in the glutamatergic system in the hippocampus contributing to the abnormal neurobehavioral outcomes.

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Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 92%

Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus

Parameshwaran

Buabeid

Karuppagounder

et al. 2011

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…[4][5][6] Both prenatal and postnatal SHS exposure in children is associated with sudden infant death syndrome, otitis media (OM), asthma, cardiovascular effects, behavioral problems, respiratory problems, and increased cancer risk. 1,[7][8][9][10][11][12][13][14][15][16] Furthermore, childhood SHS exposure is associated with increased risk of tobacco initiation [17][18][19] and symptoms of addiction in children who have never smoked. 20 There has been a sharp decline in high school students who smoke cigarettes; among 12th-grade students, 30-day prevalence rates have declined from 37% in 1997 to 14% in 2014.…”

Section: Introductionmentioning

confidence: 99%

The Difference a Decade Makes: Smoking Cessation Counseling and Screening at Pediatric Visits

Cawkwell

Lee

Shearston³

et al. 2016

NICTOB

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“…Several animal studies demonstrated that the effect of the prenatal environment can persist, influencing neuronal survival and cognitive function in the adult brain [21,22,23]. A longitudinal cross-housing study performed by Koo et al [24] showed that rats reared in a combination of prenatal and postnatal EE lasting for 3 months produced the best performance in learning and cognitive tests and displayed the highest levels of expression in brain-derived neurotrophic factor and synaptic markers in the hippocampus among the experimental groups.…”

Section: Introductionmentioning

confidence: 99%

Alteration of Energy Metabolism and Antioxidative Processing in the Hippocampus of Rats Reared in Long-Term Environmental Enrichment

Kang

Choi²,

Kim³

et al. 2016

Dev Neurosci

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Environmental enrichment (EE) is a typical experimental method that promotes levels of novelty and complexity that enhance experience-dependent neuroplasticity and cognitive behavior function in laboratory animals. Early EE is associated with resilience in the face of later-life challenges. Since increased synaptic activity enhances endogenous neuronal antioxidant defenses, we hypothesized that long-term EE beginning at an early stage may alter the levels of oxidative stress. We investigated global protein expression and oxidative stress in hippocampal proteins from rats nurtured for a 6-month EE beginning in the prenatal period. The analysis of protein expression was carried out using 2-dimensional gel electrophoresis with matrix-associated laser desorption ionization time-of-flight mass spectrometry. Proteins with altered expression were involved in energy metabolism (phosphoglycerate mutase 1, α-enolase isoform 1, adenylate kinase 1, and triose phosphate isomerase) and antioxidant enzymes (superoxide dismutase 1, glutathione S-transferase ω type 1, peroxiredoxin 5, DJ-1, and glial maturation factor β). Using Western blot assays, some of the proteins with altered expression and NADPH oxidase 2 were confirmed to be decreased. Further confirmation was demonstrated with attenuated expression of 7,8-dihydro-8-oxo-deoxyguanine, a DNA oxidative stress marker, in the hippocampus of EE group rats. Our data demonstrate that a long-term EE program beginning in the prenatal and early postnatal phase of development modulates energy metabolism and reduced oxidant stress possibly through enhanced synaptic activity. We provide evidence that EE can be developed as a tool to protect the brain from oxidative stress-induced injury.

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Late emerging effects of prenatal and early postnatal nicotine exposure on the cholinergic system and anxiety-like behavior

Cited by 62 publications

References 42 publications

Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus

Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus

The Difference a Decade Makes: Smoking Cessation Counseling and Screening at Pediatric Visits

Alteration of Energy Metabolism and Antioxidative Processing in the Hippocampus of Rats Reared in Long-Term Environmental Enrichment

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