Abstract

The role of nicotine acetylcholine receptors (nAChRs) in regulating cholinergic outflow to the airways is not fully elucidated. Furthermore, the origin of acetylcholine (ACh) or choline, as endogenous and selective agonists for nAChRs is not clear. The neurotransmitter ACh exerts its effects on the central nervous system (CNS) and peripheral nervous system (PNS) through two distinct types of receptors: the muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively). The nAChRs are involved in a wide range of physiological and pathophysiological processes. In the CNS, the nAChR system participates in multiple regulatory brain functions, including neuronal signaling, synaptic transmission and plasticity, transmitter release, development and survival of neurons, including spinal cord motor cells. In the central nervous system (CNS), there are at least 9 α (α 2–α 10) and three β (β 2– β 4) subunits. The homomeric assembly of subunits such α 7, α 8, and α 9 has been shown to be functional in mammalian cells, whereas α 2– α 6 and α 10 become operational only when co‐expressed with – β subunits. Our studies have been focused to determine the precise subunit composition and physiological roles of α 7, α 4 and β2 nAChRs in regulating upper airway dilator muscle tone. The expression of α 7, α 4, or β 2 was analyzed at the protein level, in the tissues of the rNA region, where AVPNs are located. The findings of the present study done on ferrets rNA brain region, show that AVPNs express α 7, α 4 and β 2 nAChR subunits that could assemble into functional receptors with homologous or heterologous pentameric channels.

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