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Of the more specified mechanisms by which smoking modulates the immune system is the action of nicotine or the nicotinic acetylcholine receptor α7 subunit [29].
Such an action of nicotine may contribute to the reward deficit observed during nicotine withdrawal.
Thus, the reinforcing action of nicotine in the brain, which is the driving force in nicotine addiction and tobacco smoking, should be reduced.
The experiments demonstrated above indicated a potentially important action of nicotine in perturbing the activation of G1/S checkpoints induced by γ-irradiation or BP treatment.
Therefore, the effect of smoking during pregnancy on skeletal growth may be attributed to this direct action of nicotine on growth plate chondrocytes, at least in part.
While the physiological significance of two different nAChRs both modulating hippocampal basal release of GABA could be difficult to explain their role in the mechanism of action of nicotine could be relevant.
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The connection between smoking and depression, the antidepressant actions of nicotine and the targeting of nicotinic acetylcholine receptors (nAChRs) by monoamine re-uptake inhibitors all point to a potential role of nAChRs in the etiology and/or symptomatology of depression.
Habit-forming actions of nicotine appear to be triggered primarily at nicotinic receptors on the cell bodies of dopaminergic neurons in the mesolimbic "reward" system of the brain, a region implicated in addiction to other substances including cocaine, opiates, and alcohol.
Given the putative role of serotonin in the modulation of smoking withdrawal and the central actions of nicotine, this study examined the affective and neuroelectric correlates of smoking abstinence and cigarette smoking following depletion of the serotonin precursor, tryptophan.
Indirect trophic actions of nicotine on brain during aging are suggested from observations describing nicotine as a cognitive enhancer, increasing vigilance and improving learning and memory, and both in vitro and in vivo models have demonstrated neuroprotective effects of nAChR agonists.
Employing a double-blind, placebo-controlled design, this study examined the acute actions of nicotine (6 mg) in 24 non-smokers performing a visual search task of spatial attention that was probed with behavioral performance measures and the N2pc component of the event-related potentials (ERPs), which served as a neural index of spatial attentional selection.
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