Beyond Nicotine Gateway Hypothesis_ Crimson Publishers

Beyond Nicotine Gateway Hypothesis by Somchai Bovornkitti* in Crimson Publishers: Trends in Telemedicine & E-health
Psychological studies involving humans suggested that addiction is a form of learning and that relapse is a persistent memory of the drug experiences [1,2]. It is the gene transcription factor Cyclic AMP Response-Element-Binding protein (CREB) acting as a switch, converting short-term memory to long-term memory, referred to as the acetylation of chromatin structures [3]. For nicotine gateway hypothesis, data from a group of students, aged 15.7 to 34.2 years, showing the majority of cocaine users (75.2%) were smoking during the month they began using cocaine [4], and the rate of cocaine dependence was highest (20.2%) among users who started using cocaine after having smoked cigarettes, in contrast to dependence among persons who had begun using cocaine before they started smoking (6.3%) and among those who had never smoked more than 100 cigarettes (10.1%) [5].
Combining epidemiologic and biologic studies suggest a model in which nicotine exerts the priming effect on cocaine by means of HDAC inhibition and provide a molecular explanation of the unidirectional sequence of drug use observed in mice and in human populations. Nicotine acts as a gateway drug through global acetylation in the striatum, creating an environment primed for the induction of gene expression. Long-term exposure to nicotine presumably lessens constraints on dopaminergic neurons in the ventral tegmental area and leads to the enhanced release of dopamine [6].

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