Nicotine ingested from smoking exerts neuroprotection and developmental neurotoxicity in central nervous system. It can produce changes of cognitive behaviors through regulating the release of different neurotransmitters in the brain.
However, the effects of nicotine exposure or withdrawal on neurotransmitter metabolism of hippocampal neuron still remain unclear.
Dr. LUO Qian's group from the Shenzhen Institute of Advanced Technology (SIAT) of the Chinese Academy of Sciences revealed the possible mechanism of nicotine on hippocampal dependent cognition.
Their study was published in Chinese Chemical Letters on Sept. 24.
Through a microfluidic chip-coupled with liquid chromatography-mass spectrometry (MC-LC-MS) system, the researchers evaluated the dynamic alterations in neurotransmitters metabolism of mice hippocampal neuron (HT22) cells induced by nicotine exposure and withdrawal at relevant exposure levels of smoking and secondhand smoke in real-time.
The MC-LC-MS system showed an advantage to detect unstable metabolites than conventional method by using in vitro model. "We found that HT22 cells mainly released related neurotransmitters of tryptophan and choline metabolism," said Dr. LUO.
Moreover, exposure to nicotine at relevant levels of smoking and secondhand smoke significantly altered the metabolism and secretion of serotonin, kynurenic acid, choline and acetylcholine of HT22 cells, and their alterations was closely associated with the exposure dose and duration.
These results suggested the acute exposure to nicotine was beneficial to protect the neurons, especially cognitive enhancement, and the elevated picolinic acid continually protected neuronal cognitive function after nicotine withdrawal.
Furthermore, the dynamic alterations of neurotransmitter metabolism induced by nicotine might be a possible protective mechanism of nicotine on hippocampal dependent cognition.
