ArticleJournal of neurophysiology2012
Increased nicotinic receptor desensitization in hypoglossal motor neurons following chronic developmental nicotine exposure.
Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Impacts of perinatal nicotine exposure on nicotinic acetylcholine receptor expression and glutamatergic synaptic transmission in the mouse auditory brainstem.The Journal of physiology · 2025Article
- Developmental nicotine exposure alters cardiovascular structure and function in neonatal and juvenile rats.American journal of physiology. Heart and circulatory physiology · 2024Article
- Article
- 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
- Influence of developmental nicotine exposure on serotonergic control of breathing-related motor output.Developmental neurobiology · 2022Article
- Tongue muscle contractile, fatigue, and fiber type properties in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- All roads lead to inflammation: Is maternal immune activation a common culprit behind environmental factors impacting offspring neural control of breathing?Respiratory physiology & neurobiology · 2020Review
- Selective Expression of Nicotinic Receptor Sub-unit mRNA in Early Human Fetal Forebrain.Frontiers in molecular neuroscience · 2020Article
- Diverse physiological properties of hypoglossal motoneurons innervating intrinsic and extrinsic tongue muscles.Journal of neurophysiology · 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
- 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
- Nicotinic receptor activation contrasts pathophysiological bursting and neurodegeneration evoked by glutamate uptake block on rat hypoglossal motoneurons.The Journal of physiology · 2016Article
- 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
- Enhanced corticobulbar excitability in chronic smokers during visual exposure to cigarette smoking cues.Journal of psychiatry & neuroscience : JPN · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal nicotinic acetylcholine receptors (nAChRs) are expressed on hypoglossal motor neurons (XII MNs) that innervate muscles of the tongue. Activation of XII MN nAChRs evokes depolarizing currents, which are important for regulating the size and stiffness of the upper airway. Although data show that chronic developmental nicotine exposure (DNE) blunts cholinergic neurotransmission in the XII motor nucleus, it is unclear how nAChRs are involved. Therefore, XII MN nAChR desensitization and recovery were examined in tissues from DNE or control pups using a medullary slice preparation and tight-seal whole cell patch-clamp recordings. nAChR-mediated inward currents were evoked by brief pressure pulses of nicotine or the α4β2 nAChR agonist RJR-2403. We found that, regardless of treatment, activatable nAChRs underwent desensitization, but, following DNE, nAChRs exhibited increased desensitization and delayed recovery. Similar results were produced using RJR-2403, showing that DNE influences primarily the α4β2 nAChR subtype. These results show that while some nAChRs preserve their responsiveness to acute nicotine following DNE, they more readily desensitize and recover more slowly from the desensitized state. These data provide new evidence that chronic DNE modulates XII MN nAChR function, and suggests an explanation for the association between DNE and the incidence of central and obstructive apneas.
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