processes. Of note, our analysis indicated that two pathways, synaptic long term potentiation and synaptic long term depression, were also enriched in genes associated with nicotine addiction. Repeated stimulation of nicotine to nervous system ultimately can modify the neural circuitry and thereby lead to addiction. As for many forms of experience-dependent synaptic plasticity, synaptic long term potentiation and synaptic long term depression play critical roles in the formation, maintenance, and appropriate functioning of neural circuits [41–42]. Therefore, these two pathways might be involved in the early stages of the development of nicotine addiction and facilitate the adaptation of body to changing environments. In addition, synaptic plasticity, as the molecular basis of learning and memory in the nervous system, has been extensively studied. Synaptic long term potentiation and synaptic long term depression have been reported to underline the cognitive and memory effects of the addictive potential of some drugs of abuse [43–44]. This further proved that nicotine could directly or indirectly modulate the physiological processes of learning and memory. Moreover, three signal pathways related to RXR were identified, i.e., LPS/IL-1 mediated inhibition of RXR function, PXR/RXR activation and LXR/RXR activation. Retinoic acid (RA), a class of natural or synthetic vitamin A
