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. 2016 Aug 16;3(4):ENEURO.0166-16.2016. doi: 10.1523/ENEURO.0166-16.2016

Table 5.

β2*-nAChR interacting proteins identified by iTRAQ analysis of receptors isolated from transgenic mouse cortex receiving long-term treatment with nicotine and not receiving nicotine treatment (GN, gene name)

Accession Description Correlation (r) p Value
sp|O70174|ACHA4_MOUSE Neuronal acetylcholine receptor subunit α4 OS = Mus musculus GN = Chrna4 PE = 2 SV = 2 0.97 <0.0009
sp|Q2MKA5|ACHA5_MOUSE Neuronal acetylcholine receptor subunit α5 OS = Mus musculus GN = Chrna5 PE = 2 SV = 1 0.91 <0.0009
sp|Q9ERK7|ACHB2_MOUSE Neuronal acetylcholine receptor subunit β2 OS = Mus musculus GN = Chrnb2 PE = 2 SV = 1 1 <0.0009
sp|Q6PIC6|AT1A3_MOUSE Sodium/potassium-transporting ATPase subunit α3 OS = Mus musculus GN = Atp1a3 PE = 1 SV = 1 0.55 0.042
sp|Q62277|SYPH_MOUSE Synaptophysin OS = Mus musculus GN = Syp PE = 1 SV = 2 0.59 0.026

Similar to the results from human cortex samples, presynaptic elements related to vesicle fusion (synaptophysin) and neuronal excitability (ATP1A3) are significantly correlated with nAChR levels.