ArticleRespiratory physiology & neurobiology2009
Prenatal nicotine exposure alters medullary nicotinic and AMPA-mediated control of respiratory frequency in vitro.
Article in Respiratory physiology & neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Developmental nicotine exposure alters potassium currents in hypoglossal motoneurons of neonatal rat.Journal of neurophysiology · 2017Article
- Influence of developmental nicotine exposure on glutamatergic neurotransmission in rhythmically active hypoglossal motoneurons.Experimental neurology · 2017Article
- Plasticity in respiratory motor neurons in response to reduced synaptic inputs: A form of homeostatic plasticity in respiratory control?Experimental neurology · 2017Review
- Developmental nicotine exposure disrupts dendritic arborization patterns of hypoglossal motoneurons in the neonatal rat.Developmental neurobiology · 2016Article
- Developmental nicotine exposure alters cholinergic control of respiratory frequency in neonatal rats.Developmental neurobiology · 2016Article
- Developmental nicotine exposure enhances inhibitory synaptic transmission in motor neurons and interneurons critical for normal breathing.Developmental neurobiology · 2016Article
- Influence of developmental nicotine exposure on the ventilatory and metabolic response to hyperthermia.The Journal of physiology · 2015Article
- Influence of developmental nicotine exposure on spike-timing precision and reliability in hypoglossal motoneurons.Journal of neurophysiology · 2015Article
- Neonatal nicotine exposure increases excitatory synaptic transmission and attenuates nicotine-stimulated GABA release in the adult rat hippocampus.Neuropharmacology · 2015Article
- Developmental nicotine exposure alters AMPA neurotransmission in the hypoglossal motor nucleus and pre-Botzinger complex of neonatal rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- The cellular building blocks of breathing.Comprehensive Physiology · 2012Review
- Isolated in vitro brainstem-spinal cord preparations remain important tools in respiratory neurobiology.Respiratory physiology & neurobiology · 2012Review
- Chronic neonatal nicotine exposure increases excitation in the young adult rat hippocampus in a sex-dependent manner.Brain research · 2012Article
- Increased nicotinic receptor desensitization in hypoglossal motor neurons following chronic developmental nicotine exposure.Journal of neurophysiology · 2012Article
- Developmental nicotine exposure alters neurotransmission and excitability in hypoglossal motoneurons.Journal of neurophysiology · 2011Article
- Influence of prenatal nicotine exposure on development of the ventilatory response to hypoxia and hypercapnia in neonatal rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Prenatal nicotine exposure (PNE) is correlated with breathing abnormalities in humans and other animals. Despite evidence that this relationship results from alterations in nicotinic acetylcholine receptors (nAChRs), the mechanisms are poorly understood. Here, we hypothesize that PNE blunts nAChR-mediated respiratory-related motor output. We also hypothesize that the PNE-induced changes in nAChRs leads to secondary alterations in glutamatergic neurotransmission. To test these hypotheses, we used an in vitro brainstem-spinal cord preparation and recorded C4 ventral root (C4 VR) nerve bursts from 0 to 4-day-old rats that were exposed to either nicotine (6mgkg(-1)day(-1)) or saline (control) in utero. Nicotine bitartrate, nAChR antagonists, NMDA and AMPA were applied to the brainstem compartment of a "split-bath" configuration, which physically separated the medulla from the spinal cord. Nicotine (0.2 or 0.5microM) increased peak C4 VR burst frequency by over 230% in control pups, but only 140% in PNE animals. The application of nAChR antagonists showed that these effects were mediated by the alpha4beta2 nAChR subtype with no effect on alpha7 nAChRs in either group. We also show that AMPA-mediated excitatory neurotransmission is enhanced by PNE, but NMDA-mediated neurotransmission is unaltered. These data and the work of others suggest that the PNE may functionally desensitize alpha4beta2 nAChRs located on the presynaptic terminals of glutamatergic neurons leading to less neurotransmitter release, which in turn up-regulates AMPA receptors on rhythm generating neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.