Early postnatal nicotine exposure disrupts the α2* nicotinic acetylcholine receptor-mediated control of oriens-lacunosum moleculare cells during adolescence in rats

Autor: Sakura Nakauchi, Kang Chen, Hailing Su, Katumi Sumikawa, Saki Tanimoto
Rok vydání: 2016
Předmět:
alpha 2 nicotinic acetylcholine receptor
Male
0301 basic medicine
Patch-Clamp Techniques
Long-Term Potentiation
Nicotinic Antagonists
Hippocampus
Rats
Sprague-Dawley
Nicotine
Substance Misuse
0302 clinical medicine
Pregnancy
Mecamylamine
2.1 Biological and endogenous factors
Psychology
Developmental
Nicotinic Agonists
Aetiology
Pediatric
musculoskeletal
neural
and ocular physiology
Age Factors
Gene Expression Regulation
Developmental
Valine
Long-term potentiation
Pharmacology and Pharmaceutical Sciences
OLM cells
Nicotinic acetylcholine receptor
Nicotinic agonist
Prenatal Exposure Delayed Effects
Neurological
Excitatory postsynaptic potential
Female
LTP
medicine.drug
medicine.medical_specialty
α2 nicotinic acetylcholine receptor
Development
In Vitro Techniques
Biology
Bicuculline
Inhibitory postsynaptic potential
Article
03 medical and health sciences
Cellular and Molecular Neuroscience
Interneurons
Quinoxalines
Internal medicine
Tobacco
medicine
Animals
GABA-A Receptor Antagonists
Acetylcholine receptor
Pharmacology
Neurology & Neurosurgery
Tobacco Smoke and Health
Prevention
Neurosciences
Newborn
Rats
Good Health and Well Being
030104 developmental biology
Endocrinology
Gene Expression Regulation
Animals
Newborn
nervous system
Sprague-Dawley
Drug Abuse (NIDA only)
Excitatory Amino Acid Antagonists
Neuroscience
030217 neurology & neurosurgery
Zdroj: Neuropharmacology. 101:57-67
ISSN: 0028-3908
DOI: 10.1016/j.neuropharm.2015.09.022
Popis: 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.
Databáze: OpenAIRE
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