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Activation of α2A‐containing nicotinic acetylcholine receptors mediates nicotine‐induced motor output in embryonic zebrafish
Author(s) -
Menelaou Evdokia,
Udvadia Ava J.,
Tanguay Robert L.,
Svoboda Kurt R.
Publication year - 2014
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12591
Subject(s) - nicotinic agonist , cholinergic , acetylcholine receptor , neuroscience , nicotine , nicotinic acetylcholine receptor , zebrafish , biology , acetylcholine , motor neuron , protein subunit , spinal cord , microbiology and biotechnology , receptor , endocrinology , biochemistry , gene
It is well established that cholinergic signaling has critical roles during central nervous system development. In physiological and behavioral studies, activation of nicotinic acetylcholine receptors (n AC hRs) has been implicated in mediating cholinergic signaling. In developing spinal cord, cholinergic transmission is associated with neural circuits responsible for producing locomotor behaviors. In this study, we investigated the expression pattern of the α2A n AC hR subunit as previous evidence suggested it could be expressed by spinal neurons. In situ hybridization and immunohistochemistry revealed that the α2A n AC hR subunits are expressed in spinal Rohon–Beard ( RB ) neurons and olfactory sensory neurons in young embryos. To examine the functional role of the α2A n AC h R subunit during embryogenesis, we blocked its expression using antisense modified oligonucleotides. Blocking the expression of α2A n AC hR subunits had no effect on spontaneous motor activity. However, it did alter the embryonic nicotine‐induced motor output. This reduction in motor activity was not accompanied by defects in neuronal and muscle elements associated with the motor output. Moreover, the anatomy and functionality of RB neurons was normal even in the absence of the α2A n AC hR subunit. Thus, we propose that α2A‐containing n AC hRs are dispensable for normal RB development. However, in the context of nicotine‐induced motor output, α2A‐containing n AC hRs on RB neurons provide the substrate that nicotine acts upon to induce the motor output. These findings also indicate that functional neuronal n AC hRs are present within spinal cord at the time when locomotor output in zebrafish first begins to manifest itself.