ArticleThe Journal of physiology2004
Prenatal nicotine exposure increases the strength of GABA(A) receptor-mediated inhibition of respiratory rhythm in neonatal rats.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Maternal opioids age-dependently impair neonatal respiratory control networks.Frontiers in physiology · 2023Article
- Prenatal Hypoxia Induces ClFrontiers in physiology · 2022Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- Developmental plasticity of GABAergic neurotransmission to brainstem motoneurons.The Journal of physiology · 2018Article
- Developmental nicotine exposure alters glycinergic neurotransmission to hypoglossal motoneurons in neonatal rats.Journal of neurophysiology · 2018Article
- A Novel Orally Available Asthma Drug Candidate That Reduces Smooth Muscle Constriction and Inflammation by Targeting GABAMolecular pharmaceutics · 2018Article
- Developmental nicotine exposure alters potassium currents in hypoglossal motoneurons of neonatal rat.Journal of neurophysiology · 2017Article
- Developmental nicotine exposure alters cholinergic control of respiratory frequency in neonatal rats.Developmental neurobiology · 2016Article
- Developmental nicotine exposure disrupts dendritic arborization patterns of hypoglossal motoneurons in the neonatal rat.Developmental neurobiology · 2016Article
- Evaluating the control: minipump implantation and breathing behavior in the neonatal rat.Journal of applied physiology (Bethesda, Md. : 1985) · 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
- 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
- Developmental nicotine exposure alters neurotransmission and excitability in hypoglossal motoneurons.Journal of neurophysiology · 2011Article
- Effects of postnatal smoke exposure on laryngeal chemoreflexes in newborn lambs.Journal of applied physiology (Bethesda, Md. : 1985) · 2010Article
- 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
- Prenatal nicotine exposure alters respiratory long-term facilitation in neonatal rats.Respiratory physiology & neurobiology · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infants born to mothers that smoke while pregnant have a relatively high incidence of central respiratory control abnormalities. Recent studies have shown that prenatal nicotine exposure increases GABA release and the frequency of GABAergic currents, leading to an up-regulation of GABA(A) receptors in central neurones. Activation of GABA(A) receptors inhibits ventilatory activity, with intense activation causing apnoea. These observations lead us to hypothesize that prenatal nicotine exposure alters GABAergic control of respiratory motor pattern in the early neonatal period. Osmotic minipumps were implanted in pregnant Sprague-Dawley rats on the fifth day of gestation, and filled with nicotine (6 mg kg(-1) day(-1), 2.5 microl h(-1)) or physiological saline (2.5 microl h(-1)). Brainstem-spinal cord preparations from 1- to 3-day-old neonates were studied under in vitro conditions. Electrical activity was recorded from the fourth cervical ventral root (C4 VR), which contains the axons of phrenic motoneurones. Bath application of GABA(A) receptor agonists muscimol (250 microM) or pentobarbital sodium (60 microM) to the brainstem led to consistent, reversible and significant reductions in C4 VR burst frequency. In saline-exposed animals, frequency (bursts min(-1)) fell from 6.8 +/- 0.4 to a nadir of 2.8 +/- 0.5 with muscimol, and from 6.5 +/- 0.3 to a nadir of 2.9 +/- 0.3 for pentobarbital; in nicotine-exposed animals, frequency fell from 6.3 +/- 0.4 to 1.0 +/- 0.4 with muscimol and from 6.4 +/- 0.2 to 1.7 +/- 0.4 with pentobarbital (P < 0.05 in all cases). The decrease in C4 VR frequency was significantly greater in nicotine-exposed compared to saline-exposed preparations with both muscimol and pentobarbital (P < 0.001 for both). There were no changes in the amplitude of C4 VR bursts under any condition. The GABA(A) receptor antagonist bicuculline methiodide (8 microM) did not change C4 VR frequency or amplitude in either group, although it was effective in reversing the effects of muscimol. These experiments demonstrate that prenatal nicotine exposure alters the GABAergic regulation of respiratory rhythm in a reduced preparation. The results may lead to a better understanding of the perturbed breathing pattern observed in neonates that are exposed to nicotine in utero.
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