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Article ; Online: Chronic, episodic nicotine exposure alters GABAergic synaptic transmission to hypoglossal motor neurons and genioglossus muscle function at a critical developmental age.

Wollman, Lila Buls / Flanigan, Emily Gayle / Fregosi, Ralph F

Journal of neurophysiology

2022  Volume 128, Issue 6, Page(s) 1483–1500

Abstract: Regulation of GABAergic signaling through nicotinic acetylcholine receptor (nAChR) activation is critical for neuronal development. Here, we test the hypothesis that chronic episodic developmental nicotine exposure (eDNE) disrupts GABAergic signaling, ... ...

Abstract Regulation of GABAergic signaling through nicotinic acetylcholine receptor (nAChR) activation is critical for neuronal development. Here, we test the hypothesis that chronic episodic developmental nicotine exposure (eDNE) disrupts GABAergic signaling, leading to dysfunction of hypoglossal motor neurons (XIIMNs), which innervate the tongue muscles. We studied control and eDNE pups at two developmentally vulnerable age ranges: postnatal days (P)1-5 and P10-12. The amplitude and frequency of spontaneous and miniature inhibitory postsynaptic currents (sIPSCs, mIPSCs) at baseline were not altered by eDNE at either age. In contrast, eDNE increased GABA
MeSH term(s) Humans ; Rats ; Animals ; Infant, Newborn ; Nicotine/pharmacology ; Muscimol/pharmacology ; Animals, Newborn ; Rats, Sprague-Dawley ; Synaptic Transmission/physiology ; Motor Neurons/physiology ; Tongue ; Muscles
Chemical Substances Nicotine (6M3C89ZY6R) ; Muscimol (2763-96-4)
Language English
Publishing date 2022-11-09
Publishing country United States
Document type Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID 80161-6
ISSN 1522-1598 ; 0022-3077
ISSN (online) 1522-1598
ISSN 0022-3077
DOI 10.1152/jn.00397.2022
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