English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The interaction of (±)-bupropion [(±)-BP] with the human (h) α3β4 nicotinic acetylcholine receptor (AChR) is determined by functional and structural approaches. The Ca 2+ influx results indicate that (±)-BP inhibits hα3β4 AChRs with ~2-fold lower potency than that for (±)-2-( N - tert -butylamino)-3’-iodo-4’-azidopropiophenone [(±)-SADU-3-72], indicating that this photoreactive analog can be used to further characterize the (±)-BP binding sites. The competition binding results show that (±)-BP binds to the [ 3 H]imipramine sites at desensitized hα3β4 AChRs with ~4-fold higher affinity compared to the resting state. Molecular docking results indicate that both enantiomers of BP and SADU-3-72, in the protonated state, interact with luminal and non-luminal sites. BP interacts with a luminal site which overlaps that for imipramine, and with non-luminal sites located in the transmembrane domain (TMD) at interfacial (+α3/-β4) and α3 intrasubunit sites, and in the TMD-ECD (extracellular domain) junction at the +β4/-α3 and +β4/-β4 interfaces. Our results are consistent with a hα3β4 model where BP and SADU-3-72 bind to overlapping non-luminal sites as well as non-overlapping luminal sites, probably in physiological conditions.

Bupropion inhibits human α3β4 nicotinic acetylcholine receptors by interacting with luminal and non-luminal sites