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Publication : Developmental changes in the nicotinic acetylcholine receptor in mouse tongue striated muscle.

First Author  Yamane A Year  2001
Journal  J Dent Res Volume  80
Issue  9 Pages  1840-4
PubMed ID  11926244 Mgi Jnum  J:74921
Mgi Id  MGI:2159346 Doi  10.1177/00220345010800091301
Citation  Yamane A, et al. (2001) Developmental changes in the nicotinic acetylcholine receptor in mouse tongue striated muscle. J Dent Res 80(9):1840-4
abstractText  There are no published studies on synaptogenesis focusing on the elimination of the superfluous nicotinic acetylcholine receptor (nAChR) outside the neuromuscular junction and the nAChR subunit switch from the embryonic-type (alpha2betagammadelta subunits) to the adult-type (alpha2betaepsilondelta subunits) in mouse tongues. To identify the time course of nAChR subunit elimination and switch, we analyzed the expression levels of alpha, epsilon, and gamma subunit mRNAs, and the immunolocalization of the delta subunit protein in the mouse tongue and corresponding hind limb. The analysis included the period from embryonic day (E) 11 to the newborn stage. The nAChR elimination and subunit switch began at E15 in the tongue and at E17 in the hind limb. They were nearly complete at birth in the tongue, but not in the hind limb. The early completion of synaptogenesis in the tongue at birth may be related to the early functional demands placed on the tongue, such as suckling and swallowing, immediately after birth.
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