Subsets of two groups, represented by α-neurotoxins and Lynx1, respectively, interact with nicotinic acetylcholine receptors (nAChR) and, hence, are of therapeutic interest for the treatment of neurodegenerative diseases, pain, and cancer.
Nicotine interacts with endogenous acetylcholine receptors in the brain and lung, and developmental exposure produces structural changes as well as alterations in neuroregulation.
Nicotine interacts with nicotinic acetylcholine receptors, which are present in the developing fetal brain.
Nicotine, one of the important constituents of tobacco interacts with nicotine acetylcholine receptors (nAChR) and functions in either the motor endplate of muscle or at the central nervous system for the establishment of tobacco addiction [ 10- 13].
In tobacco, there are two types of compounds that interact with neuronal nicotinic acetylcholine receptors (nnAChRs) in the brain.
Nicotine is the major toxic component of cigarette smoke and may interact with the nicotine acetylcholine receptor in many cells.
Moreover, desmin was found to directly or indirectly interact with the nicotinic acetylcholine receptor, where it has a postulated role in the submembranous organization of the motor end plate [ 117].
Further, menthol can directly interact with the nicotinic acetylcholine receptor and inhibit its function, a mechanism that may explain the reason for smoking a greater number of cigarettes to get the same effect, thereby increasing the addictive potential of nicotine.
Acetylcholine interacts with the α7-nicotinic acetylcholine receptor (α7nAChR) that is expressed in macrophages and other cells and inhibits the production of proinflammatory cytokines to attenuate the local and systemic inflammatory responses [ 7, 8].
Serotonin regulates neuronal morphology and the reconnection between neurons, 45 its pathway interacts with that of acetylcholine, 46 and it also has a role in memory impairment.
