Maternal smoking or use of other products containing nicotine during pregnancy can have significant adverse consequences for respiratory function in neonates. We have shown, in previous studies, that developmental nicotine exposure (DNE) in a model system compromises the normal function of respiratory circuits within the brainstem. The effects of DNE include alterations in the excitability and synaptic interactions of the hypoglossal motoneurons, which innervate muscles of the tongue. This study was undertaken to test the hypothesis that these functional consequences of DNE are accompanied by changes in the dendritic morphology of hypoglossal motoneurons. Hypoglossal motoneurons in brain stem slices were filled with neurobiotin during whole-cell patch clamp recordings and subjected to histological processing to reveal dendrites. Morphometric analysis, including the Sholl method, revealed significant effects of DNE on dendritic branching patterns. In particular, whereas within the first five postnatal days there was significant growth of the higher-order dendritic branches of motoneurons from control animals, the growth was compromised in motoneurons from neonates that were subjected to DNE. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1125-1137, 2016.
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http://dx.doi.org/10.1002/dneu.22379 | DOI Listing |
J Neurophysiol
January 2025
Department of Physiology, College of Graduate Studies, Midwestern University, Glendale, Arizona, United States.
Respiration is governed by a central rhythm and pattern generator, which has the pre-Bötzinger complex as the inspiratory oscillator initiating the coordinated activity of several respiratory muscles, including the diaphragm, intercostals, and upper airway muscles. The diaphragm is the main inspiratory pump muscle driving inflow, whereas dilator upper airway muscles, such as tongue muscles, reduce airway resistance during inspiration. Breathing exhibits a marked state-dependent pattern attributed to changes in neuromodulatory tone in respiratory-related brain regions, including decreases in noradrenaline and serotonin and increases in acetylcholine levels during rapid eye movement (REM) sleep.
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August 2024
Department of Pediatrics, Division of Pulmonary and Sleep Medicine, Duke University Medical Center, Durham, NC, United States.
Front Neurol
September 2024
Department of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, MO, United States.
Introduction: Tongue weakness and atrophy can lead to deficits in the vital functions of breathing and swallowing in patients with motor neuron diseases (MNDs; e.g., amyotrophic lateral sclerosis (ALS) and pseudobulbar palsy), often resulting in aspiration pneumonia, respiratory failure, and death.
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July 2024
School of Biomedical Sciences, St Lucia, QLD, Australia.
In amyotrophic lateral sclerosis (ALS) tissue and the SOD1 mouse model at mid-disease, death of hypoglossal motor neurons (XII MNs) is evident. These XII MNs innervate the intrinsic and extrinsic tongue muscles, and despite their importance in many oral and lingual motor behaviours that are affected by ALS (e.g.
View Article and Find Full Text PDFJ Neurol Sci
August 2024
Department of Neurology, Tokyo Medical University, Tokyo, Japan.
Patients with amyotrophic lateral sclerosis (ALS) do not develop oculomotor disturbances and vesicorectal dysfunction until end-stage disease owing to the survival of certain motor neurons (MNs), including oculomotor neurons and MNs within Onuf's nucleus. In sporadic ALS, adenosine deaminase acting on RNA 2 (ADAR2)-mediated editing of GluA2 mRNA at the Q/R site is compromised in lower MNs. We previously developed genetically modified mice with a conditional knockout of ADAR2 in cholinergic neurons (ADAR2/VAChT-Cre, Fast; AR2).
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