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Prenatal nicotine exposure alters intrinsic properties of neonatal hypoglossal motor neurons in the rhythmic medullary slice preparation
Author(s) -
Wakefield Hilary Ellen,
Pilarski Jason Q,
Fuglevand Andrew J,
Fregosi Ralph F
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1064.1
Subject(s) - nicotine , neuroscience , cholinergic , nicotinic agonist , electrophysiology , acetylcholine , hindbrain , medicine , respiratory system , slice preparation , anesthesia , biology , central nervous system , receptor
Hypoglossal motor neurons (HMNs) participate in a host of oromotor behaviors including swallowing and breathing. Although these neurons receive input from diverse neurotransmitter systems, of critical importance is the central cholinergic system, which participates in chemosensitivity and state changes. Prenatal nicotine exposure (PNE) reduces efficacy of nicotinic acetylcholine receptors and is associated with a variety of neonatal respiratory abnormalities. Therefore, the purpose of this study was to determine the effects of PNE on intrinsic properties of HMNs which mediate respiratory output to tongue muscles. We obtained rhythmic medullary slice preparations from P1–P4 rats exposed to saline (n = 6) or nicotine (n = 5) in utero, and we recorded from HMNs using whole cell patch clamp electrophysiology. Based on current clamp protocols applied in between respiratory bursts, we found that HMNs of PNE animals had altered firing profiles compared to HMNs of control animals. Specifically, PNE cells required 31% less current to elicit firing and had 49% higher initial frequency‐current gain values compared to control. This change in responsiveness cannot be explained by differences in input resistance. These data suggest that PNE augments HMN intrinsic excitability, which could be a result of neuroplasticity caused by chronic nicotine exposure. This study was funded by American Heart Association #0855713G.