The hypothesis that high heart rate and low perceived skill would be associated with greater return of fear than low heart rate and high perceived skill was investigated in a group of anxious musical performers (N=63) in response to an anxiety-reduction training program. Musicians were taught progressive muscle relaxation and attention-focusing skills over the course of four weekly meetings. Return of subjective fear was assessed between training program sessions and at a three-month followup assessment. The three major fear response systems were measured at pre, post and followup assessments and throughout the three training program sessions that included behavioural rehearsal. Subjects (pianists, violinists and vocalists) performed a short piece before an audience (at assessments) or before their fellow group members. Performance quality ratings by independent musicians served as the behavioural measure, anticipatory heart rate as the physiological measure, and subjective units of distress scales as the subjective measure. In addition, subjects completed memory questionnaires, designed to assess their recall of the setting and their response to previous performances, and thought questionnaires, to provide data pertinent to processes hypothesised to underlie return of fear. Four classification groups (high heart rate, low perceived skill; high heart rate, high perceived skill; low heart rate, low perceived skill; and low heart rate, high perceived skill) were formed on the basis of median splits of heart rate and perceived skill pre-assessment levels. At post-assessment, each group demonstrated fear reduction, heart rate reduced in high-heart-rate subjects, and performance quality improved overall. Followup return of fear was evident in high-heart-rate subjects regardless of initial perceived skill status, and was not dependent on initial fear levels. Perceived skill was not associated with return of fear. High-heart-rate subjects also overestimated their level of fear for previous performances, and reported more anxious thoughts and thought resensitization between performances. High non-performance heart rate was associated with greater return of fear only in extreme group analyses. Post-hoc analyses compared subjects who did (n=24) and did not (n=25) display followup return of fear. Return-of-fear subjects, in general, had higher heart rates and lower perceived skill than no-return-of-fear subjects, and tended to report thought resensitization between post and followup assessment. In addition, return-of-fear subjects were generally less skilled and performed on fewer occasions over the followup interval. The assessment of between-session return of fear was limited by design faults. The results were consistent with a dishabituation model of return of fear. They also lent support to Wagner's consolidation model in which an alteration of stimulus representations between exposures is believed to producedishabituation. The findings did not support the hypothesis that lack of consolidation may also arise from failure to attend to contextual cues, and hence, impaired retrieval of stimulus representations. Similarities of the data to Bower's description of mood-dependent cognitions were noted. It was suggested that salient internal autonomic cues during mood-congruent states facilitated overestimation of previous fear, expectation of distress and return of fear. Finally, research possibilities and treatment implications were considered. / Arts, Faculty of / Psychology, Department of / Graduate

Thesis (M.S.)--University of Delaware, 2006. / Principal faculty advisor: Michelle A. Provost-Craig, Dept. of Health, Nutrition, and Exercise Sciences. Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 7 uppsatser.

Thesis (Ph.D.)--Michigan State University. Dept. of Physiology, 2008. / Title from PDF t.p. (viewed on Mar. 27, 2009) Includes bibliographical references. Also issued in print.

Thesis (M.S.)--University of Wisconsin--Madison, 1966. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Anxiety is marked by impaired inhibition of distraction (Eysenck et al., 2007). It is unclear whether these impairments are reduced or exacerbated when loading working memory (WM) with non-affective information. Cardiac vagal control has been related to emotion regulation and may serve as a proxy for load-related inhibition under anxiety (Thayer and Lane, 2009). The present study examined whether: (1) the enhancing and impairing effects of load on inhibition exist together in a nonlinear function, (2) there is a similar association between inhibition and concurrent vagal control, (3) nonlinear relations depend on trait anxiety. During anxiogenic threat-of-noise, 116 subjects maintained a digit series of varying lengths (0, 2, 4, 6 digits) while completing a visual flanker task. The task was broken into four blocks, with a baseline period preceding each. ECG was acquired throughout to quantify vagal control as high-frequency heart rate variability (HRV). There were significant quadratic relations of WM load to flanker performance and to HRV, but no associations between HRV and performance. Trait anxiety did not moderate any relations among HRV, load, and inhibition. Results indicate that low load was associated with relatively better inhibition and increased HRV. Findings suggest that attentional performance under anxiety depends on the availability of WM resources, which might be reflected by vagal control. These results have implications for treating anxiety disorders, in which emotion regulation can be optimized for attentional focus. / Ph. D.

published_or_final_version / abstract / Biochemistry / Doctoral / Doctor of Philosophy

Cholecystokinin (CCK)-like immunoreactive materials have been localized in neurons with cell bodies in the colon and axons in the IMG of the guinea pig. The physiological significance of neuronal CCK in sympathetic prevertebral ganglia is unknown. The goal of the present studies is to test the hypothesis the CCK is a neurotransmitter in the IMG of guinea pig and rabbit. In vitro IMG preparations with or without a segment of the colon attached were utilized to conduct intracellular recordings of potentials elicited in the neurons by pressure-ejected CCK₈. The peptide triggered a depolarization with rapid onset (1-5 s) and a rate of rise (1.6 ± 0.4 mV/s) in 95% of the neurons tested. Values of the ED₅₀ for effecting depolarization average 1.1 ± 0.5 pmoles. In 59% of the cells, the depolarization was associated with a decrease in R(in) and in 20% with an increase. The remaining cells showed no change in R(in). G(Na) and G(K) were increased and decreased, respectively; potential-dependence characteristics revealed a null potential of 36 ± 9 mV in those cells exhibiting a decrease in R(in). Gastrin, caerulein, and CCK₂₇₋₃₃ effected similar depolarization. CCK₈-evoked depolarization imitated the depolarization produced either by colon distension or by nerve stimulation. Upon repeated administration of CCK₈, the response of the cells to the peptide underwent tachyphylaxis. In addition, CCK₈ desensitized the depolarization evoked by stimulation in 50% of the cells. Furthermore, in an equal percentage of neurons, CCK₈ depressed responses of the colon distension-induced depolarization. The CCK₈ has both pre- and postsynaptic sites of action is supported by lowering Ca²⁺ and administering TTX (3 μM), which caused no effect and depressed 30% of CCK-induced depolarization respectively. Spantide (SP antagonist) blocked the response to SP, but not to CCK₈, in 5 out of 6 neurons, indicating separate receptor sites for SP and CCK₈. Moveover, completely desensitizing the cell response to SP or VIP did not cross desensitize its response to CCK₈ as observed in 6 neurons. In the rabbit IMG, the physiological significance of CCK₈ excitation is unknown, since colon distension did not elicit any depolarization. These results support the hypothesis that CCK₈ or a related peptide is a neurotransmitter mediating reflex activity between the colon and the IMG in guinea pig.

This thesis examined Autonomic Nervous System activity evoked by postural instability. Autonomic reactions were assessed using measures of electrodermal activity at the surface of the skin. Perturbation-evoked electrodermal responses (EDRs) were consistently observed in conjunction with both upper and lower limb postural reactions. These autonomic responses were sensitive to perturbation amplitude, as well as experimental manipulations which did not influence the perturbation itself but which affected response execution. In particular, stimulus predictability and movement challenge modulated EDRs, although purely cognitive manipulations did not significantly affect autonomic responses. Probes examining the potential role of such autonomic potentials in compensatory balance control revealed that EDRs evoked during compensatory postural reactions were larger and more consistent than potentials evoked by purely motor or sensory stimuli, suggesting that evoked autonomic activity plays a role in compensatory behavior. While the specific role of autonomic contributions in compensatory balance control require further study, speculative models for autonomic contributions propose either feedback-based pathways for detection of instability to initiate the postural reaction, and/ or an adaptive role to higher centers important for establishing sensorimotor gain in future conditions. This thesis presents new evidence regarding basic neural mechanisms engaged in the recognition and response to postural instability, and future work may extend these findings in clinical populations with high fall incidence and offer clues as to alternative causes for falls and fall prevention.