Alexander Kuryatov

TL;DR: Overnight treatment with nicotine increased the number of nAChRs and increased the proportion of the (alpha4)(2)(beta2)(3) stoichiometry, raising the possibility for an interesting mode of synaptic regulation for nicotinic signaling in the mammalian brain.

TL;DR: It is demonstrated that nicotine can alter fetal monkey lung development by crossing the placenta to interact directly with nicotinic receptors on non-neuronal cells in the developing lung, and that similar effects likely occur in human infants whose mothers smoke during pregnancy.

TL;DR: Human neuronal nicotinic acetylcholine receptor α4 subunits and an α4 mutant found in autosomal-dominant nocturnal frontal lobe epilepsy were expressed along with β2 in permanently transfected tsA201 human embryonic kidney cell lines to investigate their sensitivity to activation, desensitization, and up-regulation by cholinergic ligands.

TL;DR: In this article, the authors investigated the functional effects of alpha 5 sub-unit co-assembly with alpha 3 and beta 2 sub-units in Xenopus oocytes and found that alpha 5 increased desensitization and Ca++ permeability of all alpha 3 AChRs.

TL;DR: The net effect of the mutation is to reduce AChR function, which could result in the hyperexcitability characteristic of epilepsy if the mutant AChRs were part of an inhibitory circuit, e.g., presynaptically regulating the release of GABA.