ArticleNeuropharmacology2016
Early postnatal nicotine exposure disrupts the α2* nicotinic acetylcholine receptor-mediated control of oriens-lacunosum moleculare cells during adolescence in rats.
Article in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Prevalence and socio-economic determinants of growth and developmental delays among Iranian children aged under five years: A cross sectional study.BMC pediatrics · 2024Article
- Nicotine on the developing brain.Pharmacological research · 2023Review
- Nicotine-mediated activation of α2 nAChR-expressing OLM cells in developing mouse brains disrupts OLM cell-mediated control of LTP in adolescence.Neurobiology of learning and memory · 2022Article
- Long-term effects of early postnatal nicotine exposure on cholinergic function in the mouse hippocampal CA1 region.Neurobiology of learning and memory · 2021Article
- Differential Effects of Nicotine Exposure on the Hippocampus Across Lifespan.Current neuropharmacology · 2018Review
- α2* Nicotinic acetylcholine receptors influence hippocampus-dependent learning and memory in adolescent mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Multiple Kinases Involved in the Nicotinic Modulation of Gamma Oscillations in the Rat Hippocampal CA3 Area.Frontiers in cellular neuroscience · 2017Article
- Impaired function of α2-containing nicotinic acetylcholine receptors on oriens-lacunosum moleculare cells causes hippocampus-dependent memory impairments.Neurobiology of learning and memory · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Maternal cigarette smoking during pregnancy and maternal nicotine exposure in animal models are associated with cognitive impairments in offspring. However, the underlying mechanism remains unknown. Oriens-lacunosum moleculare (OLM) cells expressing α2* nicotinic acetylcholine receptors (nAChRs) are an important component of hippocampal circuitry, gating information flow and long-term potentiation (LTP) in the CA1 region. Here we investigated whether early postnatal nicotine exposure alters the normal role of α2*-nAChR-expressing OLM cells during adolescence in rats. We found that early postnatal nicotine exposure significantly decreased not only the number of α2-mRNA-expressing interneurons in the stratum oriens/alveus, but also α2*-nAChR-mediated responses in OLM cells. These effects of nicotine were prevented by co-administration with the nonselective nAChR antagonist mecamylamine, suggesting that nicotine-induced activation, but not desensitization, of nAChRs mediates the effects. α2*-nAChR-mediated depolarization of OLM cells normally triggers action potentials, causing an increase in spontaneous inhibitory postsynaptic currents in synaptically connected pyramidal cells. However, these α2*-nAChR-mediated effects were profoundly reduced after early postnatal nicotine exposure, suggesting altered control of CA1 circuits by α2*-nAChR-expressing OLM cells. Furthermore, these effects were associated with altered excitatory neural activity and LTP as well as the loss of normal α2*-nAChR-mediated control of excitatory neural activity and LTP. These findings suggest the altered function of α2*-nAChR-expressing OLM cells as an important target of further study for identifying the mechanisms underlying the cognitive impairment induced by maternal smoking during pregnancy.
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