Nicotine Improves Working Memory via Augmenting BDNF Levels Through α7 nAChR: Evidence from Clinical and Preclinical...

While smoking has been associated with many negative consequences to human health, one possible benefit is that nicotine could improve cognitive functions. Previous studies have suggested that smoking may influence brain-derived neurotrophic factor (BDNF) levels. However, the exact effects of smoking on BDNF and cognition, and the potential neurobiological mechanisms underlying the changes induced by nicotine, remain elusive.

Two tobacco products were used in the population to detect plasma BDNF, and the spatial memory was examined using the N-back test. Acute and chronic nicotine exposure and withdrawal models were established in rats. BDNF levels and relevant targets in serum, cerebrospinal fluid, and hippocampus were detected, and spatial memory and motor ability were evaluated by Y-maze test. Pharmacological blockage or genetic deletion of α7 nicotinic acetylcholine receptors (nAChR) was administered to rats to confirm its role in regulating the effects of nicotine on BDNF and memory levels.

Our research revealed that tobacco product use led to an increase in working memory and human plasma BDNF levels. Furthermore, nicotine was responsible for the elevation in BDNF levels, which showed dose-dependent increases in both serum and the hippocampus, and improved memory performance. Conversely, BDNF levels decreased with prolonged withdrawal from nicotine, and resulted in impaired memory performance. However, when the α7 nAChR was inhibited by the receptor antagonist methyllycaconitine citrate (MLA) or genetic knockout, the elevation of BDNF levels caused by chronic nicotine exposures was blocked.

The nicotine in tobacco can improve memory through α7 nAChR.