ArticleJournal of neurophysiology2011
Developmental nicotine exposure alters neurotransmission and excitability in hypoglossal motoneurons.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 39 citations in OpenAlex.
- Chronic, episodic nicotine exposure alters GABAergic synaptic transmission to hypoglossal motor neurons and genioglossus muscle function at a critical developmental age.Journal of neurophysiology · 2022Article
- Prenatal nicotine alters development of the laterodorsal tegmentum: Possible role for attention-deficit/hyperactivity disorder and drug dependence.World journal of psychiatry · 2022Review
- Homeostatic Regulation of Motoneuron Properties in Development.Advances in neurobiology · 2022Review
- Tongue muscle contractile, fatigue, and fiber type properties in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Cellular and Molecular Changes in Hippocampal Glutamate Signaling and Alterations in Learning, Attention, and Impulsivity Following Prenatal Nicotine Exposure.Molecular neurobiology · 2020Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- Diverse physiological properties of hypoglossal motoneurons innervating intrinsic and extrinsic tongue muscles.Journal of neurophysiology · 2019Article
- Cell death in the human infant central nervous system and in sudden infant death syndrome (SIDS).Apoptosis : an international journal on programmed cell death · 2019Article
- 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
- Perinatal nicotine exposure impairs the maturation of glutamatergic inputs in the auditory brainstem.The Journal of physiology · 2017Article
- 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 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
- Activity-dependent plasticity in the isolated embryonic avian brainstem following manipulations of rhythmic spontaneous neural activity.Respiratory physiology & neurobiology · 2016Article
- Intrinsic excitability differs between murine hypoglossal and spinal motoneurons.Journal of neurophysiology · 2016Article
- Developmental nicotine exposure enhances inhibitory synaptic transmission in motor neurons and interneurons critical for normal breathing.Developmental neurobiology · 2016Article
- Current injection and receptor-mediated excitation produce similar maximal firing rates in hypoglossal motoneurons.Journal of neurophysiology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hypoglossal motoneurons (XII MNs) control muscles of the mammalian tongue and are rhythmically active during breathing. Acetylcholine (ACh) modulates XII MN activity by promoting the release of glutamate from neurons that express nicotinic ACh receptors (nAChRs). Chronic nicotine exposure alters nAChRs on neurons throughout the brain, including brain stem respiratory neurons. Here we test the hypothesis that developmental nicotine exposure (DNE) reduces excitatory synaptic input to XII MNs. Voltage-clamp experiments in rhythmically active medullary slices showed that the frequency of excitatory postsynaptic currents (EPSCs) onto XII MNs from DNE animals is reduced by 61% (DNE = 1.7 ± 0.4 events/s; control = 4.4 ± 0.6 events/s; P < 0.002). We also examine the intrinsic excitability of XII MNs to test whether cells from DNE animals have altered membrane properties. Current-clamp experiments showed XII MNs from DNE animals had higher intrinsic excitability, as evaluated by measuring their response to injected current. DNE cells had high-input resistances (DNE = 131.9 ± 13.7 MΩ, control = 78.6 ± 9.7 MΩ, P < 0.008), began firing at lower current levels (DNE = 144 ± 22 pA, control = 351 ± 45 pA, P < 0.003), and exhibited higher frequency-current gain values (DNE = 0.087 ± 0.012 Hz/pA, control = 0.050 ± 0.004 Hz/pA, P < 0.02). Taken together, our data show previously unreported effects of DNE on XII MN function and may also help to explain the association between DNE and the incidence of central and obstructive apneas.
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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.