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Nicotinic Enhancement of Incentive Salience

Description
Incentive salience is a motivational-cognitive process that can transform an otherwise neutral stimulus into something that is wanted. The prolonged use of nicotine appears to enhance incentive salience; it has been suggested that the nicotinic enhancement of incentive salience contributes to the potential of relapse in individuals with tobacco addiction.…

Incentive salience is a motivational-cognitive process that can transform an otherwise neutral stimulus into something that is wanted. The prolonged use of nicotine appears to enhance incentive salience; it has been suggested that the nicotinic enhancement of incentive salience contributes to the potential of relapse in individuals with tobacco addiction. In order to determine whether (a) nicotinic enhancement of incentive salience for non-nicotinic stimuli occurs when rats self-administer nicotine and (b) a history of nicotine use facilitates such enhancement, rats were trained in a morning self-administration paradigm (SA), in combination with an afternoon 4-CS Pavlovian conditioned approach task (PCA) for 24 days. SA was followed by extinction and cue reinstatement. Nicotine SA enhanced incentive salience in the PCA. Upon extinction, incentive salience quickly declined to saline levels, indicating that the nicotinic enhancement of incentive salience is transient. Experimenter-administered nicotine enhanced incentive salience similarly regardless of nicotine history, suggesting that a previous history of nicotine use does sensitize the nicotinic enhancement of incentive salience. Taken together, these results suggest that nicotine must be onboard for the expression of nicotinic enhancement of incentive salience. This suggests that the role of incentive salience in the development and relapse of tobacco addiction may need to be revisited.
ContributorsOverby, Paula F. (Author) / Sanabria, Federico (Thesis director) / Gipson-Reichardt, Cassandra (Committee member) / Beckmann, Joshua (Committee member) / School of Life Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
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The role of nucleus accumbens NMDA receptors on rapid, transient synaptic plasticity induced by cued nicotine reinstatement

Description
Nicotine use is an outstanding public health problem with associated social and economic consequences. Nicotine is an active alkaloid compound in tobacco and is recognized as a psychoactive drug. Preclinically, nicotine addiction and relapse can be modeled using a self-administration-reinstatement paradigm. Here, we used a nicotine self-administration and contingent cue-induced…

Nicotine use is an outstanding public health problem with associated social and economic consequences. Nicotine is an active alkaloid compound in tobacco and is recognized as a psychoactive drug. Preclinically, nicotine addiction and relapse can be modeled using a self-administration-reinstatement paradigm. Here, we used a nicotine self-administration and contingent cue-induced reinstatement model to examine rapid, transient synaptic plasticity (t-SP) induced by nicotine cue-triggered motivation. Although preliminary, treatment with the NMDA GluN2B subunit antagonist, ifenprodil, reduced reinstated nicotine seeking, and increased the percentage of spines with smaller head diameters. Thus, future studies are needed to fully parse out the role of NAcore GluN2B receptors in cued nicotine seeking and t-SP.
ContributorsMccallum, Joseph John (Author) / Gipson-Reichardt, Cassandra (Thesis director) / Neisewander, Janet (Committee member) / Olive, Michael Foster (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
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Suppressive and Enhancing Effects of Nicotine on Food-Seeking Behavior

Description
The present study examined how systemic low doses of nicotine affect the microstructure of food-reinforced behavior in rats. Rats were given an acute saline or nicotine treatment (0.1-0.6 mg/kg, resting at least 48 h between injections), and a chronic saline or nicotine treatment (0.3 mg/kg for 10 consecutive days). Immediately…

The present study examined how systemic low doses of nicotine affect the microstructure of food-reinforced behavior in rats. Rats were given an acute saline or nicotine treatment (0.1-0.6 mg/kg, resting at least 48 h between injections), and a chronic saline or nicotine treatment (0.3 mg/kg for 10 consecutive days). Immediately after treatment, rats were required to press a lever to obtain food, whose availability was unpredictable, but programmed at a constant rate (on average every 80 s). Acute nicotine dose-dependently suppressed behavior prior to the delivery of the first reinforcer, but enhanced food-reinforced behavior afterwards. This effect was primarily observed in the time it took rats to initiate food-seeking behavior, and not in the food-seeking behavior itself. A pre-feeding control procedure suggests that these effects cannot be explained only by changes in appetite. Over the course of chronic nicotine exposure, tolerance developed to the suppressive, but not to the enhancing effects of nicotine on food-seeking behavior. These results suggest that ostensive sensitization effects of nicotine on behavior may instead reflect a tolerance for its suppressive effects on behavior.
ContributorsRomero, Korinna Estela (Author) / Sanabria, Federico (Thesis director) / Gipson-Reichardt, Cassandra (Committee member) / Bevins, Rick (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05