The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Molecular effects of dimethylanatoxin on the peripheral nicotinic acetylcholine receptor.

N,N-dimethylanatoxin (DMAnTX), the quaternary derivative of the potent nicotinic agonist (+)-anatoxin-a (AnTX), has been evaluated for potency and efficacy at nicotinic acetylcholine receptors of frog motor endplates and Torpedo electric organs. DMAnTX was only weakly effective in eliciting contracture of the frog rectus abdominis and was orders of magnitude less potent than AnTX. Biochemical assay showed that DMAnTX was a weak inhibitor of [125I]alpha-bungarotoxin binding to the receptors in frog muscle and Torpedo electroplaque membranes: the IC50 values were 60 and 14 microM, respectively. A low frequency of single channel currents recorded from isolated interosseal fibers at concentrations from 20 to 100 microM of DMAnTX and the stimulation of [3H]perhydrohistrionicotoxin [( 3H]H12-HTX) binding (half-maximal at 0.3 microM) confirmed the weak activation of the receptor. DMAnTX also exhibited antagonist effects. In muscle twitch assays, 100 microM of DMAnTX effectively decreased the tension induced by nerve stimulation, although DMAnTX did not affect muscle membrane action potentials. The binding of [3H] perhydrohistrionicotoxin was also inhibited at high micromolar concentrations of DMAnTX. Combination of DMAnTX with acetylcholine in single channel current experiments demonstrated that DMAnTX possesses ion channel blocking properties, which become apparent at low micromolar concentrations, and DMAnTX enhances the desensitization induced by acetylcholine above 10 microM AnTX. The difference in agonist potency between AnTX and DMAnTX may be attributed to a change in conformation of the molecular skeleton induced by the N-methyl groups.[1]


  1. Molecular effects of dimethylanatoxin on the peripheral nicotinic acetylcholine receptor. Costa, A.C., Swanson, K.L., Aracava, Y., Aronstam, R.S., Albuquerque, E.X. J. Pharmacol. Exp. Ther. (1990) [Pubmed]
WikiGenes - Universities