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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Postnatal nicotine effects on the expression of nicotinic acetylcholine receptors in the developing piglet
Arunnjah Vivekanandarajah1, Karen A Waters2, Rita Machaalani2
1The BOSCH Institute, NSW 2006, Australia; Department of Medicine, Blackburn Building, DO6, University of Sydney, NSW 2006, Australia.
Insights
Postnatal nicotine exposure alters brain nicotinic acetylcholine receptor (nAChR) subunits in piglets, impacting cardiorespiratory control and cognition. This study reveals critical developmental neurotoxicity from environmental smoke exposure.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Postnatal exposure to cigarette smoke is linked to infant respiratory illnesses, SIDS, and childhood cognitive deficits.
- Nicotine, a key component of cigarette smoke, exerts neurotoxic effects by interacting with nicotinic acetylcholine receptors (nAChRs).
Purpose of the Study:
- To investigate the impact of postnatal nicotine exposure on the expression of specific nAChR subunits in the developing piglet brain.
- To examine changes in nAChR subunit expression in the hippocampus (cognition) and brainstem medulla (cardiorespiratory control).
Main Methods:
- Utilized a piglet model for controlled postnatal nicotine exposure (2mg/kg/day for 14 days).
- Employed immunohistochemistry to analyze the expression of nAChR subunits (α2, α3, α4, α5, α7, α9, β1, β2) in the hippocampus and brainstem medulla.
- Compared nicotine-exposed piglets to a control group.
Main Results:
- Significant alterations in nAChR subunit expression were observed in both brain regions.
- In the hippocampus, decreased expression of α3, α9, β1, and β2 subunits was noted.
- In the medulla, specific nuclei showed increased (α2, α4) or decreased (α3, α4, β1) expression of various nAChR subunits.
Conclusions:
- This study provides the first evidence that non-classical nAChR subunits are affected by postnatal nicotine exposure during critical brain development.
- Observed changes suggest potential mechanisms underlying the neurodevelopmental and cardiorespiratory consequences of infant smoke exposure.
Abstract:
Postnatal exposure to cigarette smoke during infancy is associated with increased number of respiratory illnesses, impaired pulmonary function, and the occurrence of Sudden Infant Death Syndrome (SIDS). It is also associated with reduced cognitive functioning and attention deficits in childhood. Nicotine, the major neurotoxic component of cigarette smoke, induces its actions by binding to nicotinic acetylcholine receptors (nAChR). Using a piglet model of postnatal nicotine exposure, we studied the immunohistochemical expression of nAChR subunits α2, α3, α4, α5, α7, α9, β1 and β2 in the brainstem medulla and the hippocampus, given the role of these structures in cardiorespiratory control and cognition, respectively. We compared piglets exposed postnatally to 2mg/kg/day nicotine for 14 days (n=14: 7 males: 7 females) to controls (n=14: 7 males: 7 females). In the hippocampus, decreased expression was seen for α3 in CA1 (p=0.017), α9 in CA1 (p<0.001) and CA2 (p<0.001), β1 in CA1 (p=0.001) and CA2 (p=0.001) and β2 in CA3 (p=0.036). In the medulla, the nucleus of the spinal trigeminal tract had increased α2 and α4; vestibular nucleus increased α2 and α3, and decreased α4; hypoglossal decreased α3 and β1; dorsal motor nucleus of the vagus decreased α4 and β1. This is the first demonstration that non-classical nAChR subunits are affected by postnatal nicotine in the developing brain, and the implications are discussed.
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