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dc.creatorBorowski, Thomas Brianen_US
dc.date.accessioned2004-10-21T00:08:03Zen_US
dc.date.accessioned2013-01-04T05:03:24Z
dc.date.available1997-04-01T08:00:00Zen_US
dc.date.available2013-01-04T05:03:24Z
dc.date.created1997-04en_US
dc.date.issued1997-04-01en_US
dc.date.submittedApril 1997en_US
dc.identifier.urihttp://hdl.handle.net/10388/etd-10212004-000803en_US
dc.description.abstractThe involvement of dopamine (DA) in the emotional and psychiatric disturbances associated with schizophrenia and psychomotor stimulant abuse is well known; however, the mechanism by which DA mediates fear expression and anxiety is not well defined. Accordingly, the objective of the present thesis was to determine the fear-motivational functions of DA neurons in the ventral tegmental area (VTA) and to examine the role of DA in fear extinction using the potentiated startle paradigm. In Experiment 1, it was observed that electrical stimulation of the VTA produced a pronounced increase in the amplitude of the acoustic startle reflex. In subsequent experiments fear-potentiated startle was assessed following axon-sparing N-methyl-D-aspartic acid (NMDA) lesions of the VTA and after bilateral intra-VTA infusion of the DA D2/3 receptor agonist quinpirole (Experiments 2-4). The NMDA lesions resulted in substantial cell loss in the medial ventral tegmentum and blocked fear-potentiated startle. Similarly, inhibition of DA neuronal activity associated with locally-administered quinpirole suppressed the expression of the conditioned fear-induced increase in startle amplitudes. The quinpirole results implicate DA neuronal functioning in fear motivation. To explore further the involvement of DA in aversive emotional behavior, pharmacological experiments were conducted in which the effects of peripherally-administered DA agonist drugs on fear extinction were assessed. Subjects in Experiment 5 received an acute injection of either cocaine hydrochloride (40.0 mg/kg), d-amphetamine sulphate (5.0 mg/kg), the D2/3 agonist quinpirole hydrochloride (5.0 mg/kg), or the D1-type agonist SKF 38393 (5.0 mg/kg) during a single extinction session following fear acquisition. Animals treated with cocaine, d-amphetamine, and SKF 38393 exhibited fear-potentiated startle, whereas quinpirole treatment failed to alter fear extinction to the nonreinforced conditioned stimulus (CS). Also, it was revealed using a within-subjects design in Experiment 6 that cocaine administration reinstated fear-potentiated startle following extinction. Taken together, the results of the present experiments suggests fundamental role for DA and DA D1 receptors in fear expression. It was proposed that VTA DA neurons gate levels of aversive emotional arousal within the amygdala-based fear system.en_US
dc.language.isoen_USen_US
dc.subjectventral tegmental area (VTA)en_US
dc.subjectamygdalaen_US
dc.subjectrats - neurochemistryen_US
dc.subjectpsychologyen_US
dc.subjectdopamine neuronsen_US
dc.subjectfear motivationen_US
dc.titleThe role of ventral tegmental dopamine neurons and the effects of central and peripheral dopamine agonists on fear motivation as measured by the potentiated acoustic startle reflex in ratsen_US
thesis.degree.departmentPsychologyen_US
thesis.degree.disciplinePsychologyen_US
thesis.degree.grantorUniversity of Saskatchewanen_US
thesis.degree.levelDoctoralen_US
thesis.degree.nameDoctor of Philosophy (Ph.D.)en_US
dc.type.materialtexten_US
dc.type.genreThesisen_US
dc.contributor.committeeMemberCheesman, James E. (Jim)en_US


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