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A rat model of novelty-seeking phenotype predicts vulnerability to nicotine relapse where locomotor reactivity to novelty is used to rank high (HR) versus low (LR) responders. This dissertation examines the neuropeptidergic and structural substrates of the expression of locomotor sensitization to a low dose nicotine challenge and associated social anxiety-like behavior following chronic intermittent nicotine exposure during adolescence in the LRHR phenotype. Data show the long-lasting nature of behavioral sensitization to nicotine and abstinence-related social anxiety-like behavior in nicotine pre-trained HRs compared to saline pre-trained controls. Moreover, this behavior is accompanied by an imbalance between the brain antistress/antianxiety, i.e., neuropeptide Y (NPY), and stress, i.e., corticotrophin releasing factor (CRF) systems in the amygdala. Moreover, a deficit in NPY signaling marked with decreased NPY and increased NPY Y2 receptor (Y2R) mRNA levels is observed in the hip pocampus, along with mossy fiber reorganization in nicotine pre-trained HRs. Furthermore, a Y2R antagonist administered 1 wk of abstinence reverses these behavioral, molecular and morphological effects in nicotine-exposed HRs. Additionally, the role of amygdalar synaptic plasticity in longlasting social withdrawal is also investigated by assessing brain-derived neurotrophic factor (BDNF) and spinophilin mRNA levels in HRs following a behaviorally-sensitizing nicotine regimen. A persistent increase in BDNF and spinophilin mRNA levels in the basolateral amygdala (BLA) is observed in nicotine pre-trained HRs even across a long (3-wk) abstinence spanning into young adulthood. This strongly suggests BDNFmediated long-lasting neuroplasticity within the BLA that may regulate abstinence-related negative affect in HRs. / Moreover, a cannabinoid receptor 1 (CB1R) antagonist, AM251 treatment during a short (1-wk) abstinence is ineffective in reversing social anxiety, nicotine-induced neuroplasticity and the neuropeptidergic changes in the amygdala, although it is effective in reversing the expression of locomotor sensitization to challenge nicotine even following a long (3-wks) abstinence. Furthermore, the identical AM251 treatment given during the late phase of a long (3-wk) abstinence further augments social withdrawal and associated BLA plasticity in nicotine pre-trained HRs. These findings implicate neuropeptidergic and neuroplastic changes in the hippocampus and the amygdala in vulnerability to the long-lasting behavioral effects of nicotine in the novelty-seeking phenotype. / by Cigdem Aydin. / Thesis (Ph.D.)--Florida Atlantic University, 2011. / Includes bibliography. / Electronic reproduction. Boca Raton, Fla., 2011. Mode of access: World Wide Web.

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Eight experiments tested priming in short-term memory as a model for latent inhibition and habituation. The model postulates that the two phenomena result from reduced processing when a representation of the target stimulus is already active (primed) in short-term memory at the time of its presentation. Priming is assumed to depend on the integrity of an association formed between the contextual stimuli and the conditional stimulus (CS) during exposure. Using a procedure that should have overshadowed the context, Experiment 1 found that latent inhibition and habituation were nevertheless maintained when a second CS of either equal or shorter duration overlapped with the target during exposure. Experiment 2 found no support for the priming of a configural stimulus when simultaneous compounds were preexposed. Experiment 3 ruled out sensitization and/or pseudoconditioning as an alternative explanation of latent inhibition. Experiments 4, 5 and 6 showed that sensory preconditioning as well as habituation and latent inhibition were obtained with compound exposure, providing evidence that the added CS was indeed processed along with the target. In Experiment 7, sequential pairings produced as much latent inhibition as compounds but less sensory preconditioning. Experiment 8 showed that retardation of conditioned inhibition was not attenuated by compound exposure. These results are interpreted as consistent with a correlational approach to classical conditioning.

Thesis (M.S.)--University of Wisconsin--Madison, 1982. / Typescript. Includes bibliographical references (leaves 133-144).

Thesis (M.A.)--University of British Columbia, 2003. / Includes bibliographical references (leaves 154-170).

Behavior analysts refer to a decrease in response rate following repeated, contingent presentations of a reinforcing stimulus as a product of satiation. Other evidence suggests that these decreases may often be due to habituation to the sensory properties of the reinforcing stimulus. The investigation reported here sought to determine whether decreases in operant responding by 3 adults with developmental disabilities were due to satiation or habituation. During baseline, participants placed poker chips into a container, and no reinforcement was available. Within subsequent phases, participants received diet lemon-lime soda on a fixed-ratio (FR) schedule of reinforcement. In one condition, the color of the soda was constant throughout the session, and in another condition food coloring was added several minutes into the session. Results for at least 2 participants indicated that: (a) soda functioned as a reinforcer for placing poker chips in the can; (b) response rates decreased within the session to baseline levels; and (c) response rates increased following a change in the color of the soda within the session. Results for the third participant were less clear. The results support the argument made by other researchers that the terms habituation (a weakening of a behavior following contact with the reinforcing stimulus) and stimulus specificity (a strengthening of a behavior following a change in the reinforcing stimulus) may be more appropriate descriptors of within-session changes in responding. The factors associated with habituation and satiation, as well as both basic and applied research examples, are discussed.

Repetitive presentation of any non-significant stimulus to an animal results in a decrement in the animal's response to that stimulus. This phenomenon, termed habituation, is distinguishable from fatigue and receptor adaptation in that it is long-lasting and in that the habituation is fairly specific to the repeated stimulus. The prevailing view of habituation is that it, like learning in general, results from an increase in the efficacy of neural transmission, but, unlike learning, this increased efficacy primarily affects inhibitory interneurons (e.g., Soko1ov, 1960; Hernandez-Peon, 1960; Jouvet, 1961). Within this broad framework, disagreements exist regarding the source of the inhibitory influences. [...]

Thesis (Ph. D.)--State University of New York at Binghamton, Department of Psychology, 2008. / Includes bibliographical references.

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