Abstract
While various modalities of chronic nicotine use have been associated with numerous negative consequences to human health, one possible benefit of nicotine exposure has been uncovered. The discovery of an inverse correlation between smoking and Parkinson’s disease, and later Alzheimer’s disease as well, motivated investigation of nicotine as a neuroprotective agent. Some studies have demonstrated that nicotine elicits improvements in cognitive function. The hippocampus, along with the subventricular zone (SVZ), is a distinct brain region that allow for ongoing postnatal neurogenesis throughout adulthood and plays a major role in certain cognitive behaviors like learning and memory. Therefore, one hypothesis underlying nicotine-induced neuroprotection is possible effects on neural stem cells and neural precursor cells. On the other hand, nicotine withdrawal frequently leads to cognitive impairments, particularly in hippocampal-dependent behaviors, possibly suggesting an impairment of hippocampal neurogenesis with nicotine exposure. This review discusses the current body of evidence on nicotine’s effects on neural stem cells and neural progenitors. Changes in neural stem cell proliferation, survival, intracellular dynamics, and differentiation following acute and chronic nicotine exposure are examined.
Highlights
Neurogenesis in the adult mammalian brain primarily occurs in two distinct regions: the subventricular zone (SVZ) located along the walls of the lateral ventricles and the subgranular zone (SGZ) located in the dentate gyrus (DG) of the hippocampus
Generated neural progenitor cells (NPCs) in the SVZ give rise to another type of neural precursor called the migrating neuroblast, which travel from the lateral ventricles to the olfactory bulb (OB) along the rostral migratory stream (RMS) where they mature into neural cells involved in olfaction [7,8,9,10,11,12]
Studies have shown abstinence from smoking in nicotine-dependent individuals leads to profound cognitive impairment [28,29,30] and disruption of hippocampal and prefrontal cortex (PFC) associated behaviors [31,32,33,34,35], suggesting that chronic nicotine exposure might impair or otherwise alter mechanisms related to learning and memory such as hippocampal neurogenesis
Summary
Neurogenesis in the adult mammalian brain primarily occurs in two distinct regions: the subventricular zone (SVZ) located along the walls of the lateral ventricles and the subgranular zone (SGZ) located in the dentate gyrus (DG) of the hippocampus. Generated NPCs in the SVZ give rise to another type of neural precursor called the migrating neuroblast, which travel from the lateral ventricles to the olfactory bulb (OB) along the rostral migratory stream (RMS) where they mature into neural cells involved in olfaction [7,8,9,10,11,12] Because both clinical and preclinical studies have demonstrated that nicotine elicits improvements in cognitive function [13,14,15,16,17,18,19] and possibly offers neuroprotection against neurodegenerative conditions [20,21], many studies have sought to elucidate the effect of nicotine on neuroplasticity. As brain development continues into the mid-twenties, elucidation of the neurological consequences of nicotine exposure is paramount [38,39]
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