Although neuroadaptations in the nucleus accumbens (NAc) are thought to contribute to nicotine addiction, little is known about the chronic effects of nicotine on NAc neuronal activity. In the present experiment, rats were exposed to a 23-day period of nicotine self-administration (SA), a 30-day abstinence period, and a 7-day period of re-exposure to SA. Chronic electrophysiological procedures were used to record the activity of individual NAc neurons on the 3rd and 23rd day of initial SA and on the 1st, 3rd, and 7th day of re-exposure. Between-session comparisons showed that NAc neurons exhibit two patterns of plasticity under the present experimental conditions. First, phasic-increase firing patterns time-locked to the nicotine-reinforced lever-press do not change during initial SA, but then show increases in prevalence and amplitude post-abstinence, which persist during re-exposure. Second, for neurons that show no phasic response time-locked to the nicotine-reinforced lever-press, average baseline and SA firing rates decrease during initial SA, return to normal during abstinence, and decrease again during re-exposure. As a combined consequence of the two types of neurophysiological plasticity, average firing rate of NAc neurons at the time of nicotine-directed behavior undergoes a progressive and persistent net amplification, across the successive stages of SA, abstinence, and re-exposure. This net increase in NAc firing at the time of nicotine-directed behavior occurs with an increase in animals’ motivation to seek nicotine. The adaptations which occur in nicotine-exposed animals do not occur in animals exposed to sucrose. The NAc neurophysiological plasticity potentially contributes to compulsive tobacco use.
Keywords: extracellular recording, nicotine addiction, self-administration, abstinence, nucleus accumbens, neuroadaptation