Neonatal nicotine exposure increases excitatory synaptic transmission and attenuates nicotine-stimulated GABA release in the adult rat hippocampus
| Autor: | William H. Griffith, Joanne C. Damborsky, Ursula H. Winzer-Serhan |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Nicotine Patch-Clamp Techniques Glutamic Acid Pharmacology Neurotransmission Biology Synaptic Transmission Article Rats Sprague-Dawley Tissue Culture Techniques Cellular and Molecular Neuroscience Glutamatergic Excitatory synapse medicine Animals Nicotinic Agonists Receptors AMPA CA1 Region Hippocampal gamma-Aminobutyric Acid Dose-Response Relationship Drug Pyramidal Cells Miniature Postsynaptic Potentials Glutamate receptor Excitatory Postsynaptic Potentials Nicotinic acetylcholine receptor Nicotinic agonist Animals Newborn Inhibitory Postsynaptic Potentials GABAergic medicine.drug |
| Zdroj: | Neuropharmacology. 88:187-198 |
| ISSN: | 0028-3908 |
| DOI: | 10.1016/j.neuropharm.2014.06.010 |
| Popis: | Developmental exposure to nicotine has been linked to long-lasting changes in synaptic transmission which may contribute to behavioral abnormalities seen in offspring of women who smoke during pregnancy. Here, we examined the long-lasting effects of developmental nicotine exposure on glutamatergic and GABAergic neurotransmission, and on acute nicotine-induced glutamate and GABA release in the adult hippocampus, a structure important in cognitive and emotional behaviors. We utilized a chronic neonatal nicotine treatment model to administer nicotine (6 mg/kg/day) to rat pups from postnatal day (P) 1–7, a period that falls developmentally into the third human trimester. Using whole-cell voltage clamp recordings from CA1 pyramidal neurons in hippocampal slices, we measured excitatory and inhibitory postsynaptic currents in neonatally control- and nicotine-treated young adult males. Neonatal nicotine exposure significantly increased AMPA receptor-mediated spontaneous and evoked excitatory signaling, with no change in glutamate release probability in adults. Conversely, there was no increase in spontaneous GABAergic neurotransmission in nicotine-males. Chronic neonatal nicotine treatment had no effect on acute nicotine-stimulated glutamate release in adults, but acute nicotine-stimulated GABA release was significantly attenuated. Thus, neonatal nicotine exposure results in a persistent net increase in excitation and a concurrent loss of nicotinic acetylcholine receptor (nAChR)-mediated regulation of presynaptic GABA but not glutamate release, which would exacerbate excitation following endogenous or exogenous nAChR activation. Our data underscore an important role for nAChRs in hippocampal excitatory synapse development, and suggest selective long-term changes at specific presynaptic nAChRs which together could explain some of the behavioral abnormalities associated with maternal smoking. This article is part of the Special Issue entitled ‘GABAergic Signaling in Health and Disease’. |
| Databáze: | OpenAIRE |
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