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Title: Investigating the effects of psychosocial stress on cerebellar function
Author: Gheorghe, Delia
ISNI:       0000 0004 7654 2252
Awarding Body: University of East Anglia
Current Institution: University of East Anglia
Date of Award: 2018
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Differences in cerebellar structure and function are consistently reported in individuals exposed to early-life stress and individuals with diagnosed stress-related psychopathology. Despite this, current neurobiological models of stress have not considered the role of the cerebellum in the regulation of the stress response. Furthermore, it is unclear the mechanism by which stress may affect cerebellar function. The studies presented in this thesis set out to address these questions by exploring the relationship between acute psychosocial stress and the cerebellum. To achieve this, two putative cerebellar functions were investigated: saccadic adaptation and postural balance control. Chapters 4 and 5 present two studies, which evaluated the effectiveness of each task, as well as individual differences in task performance. Chapter 4 presents evidence demonstrating a linear effect of saccadic adaptation across participants. Chapter 5 revealed improved postural balance control under perturbed balancing conditions. Individual differences in task performance were inconclusive. Each study was followed by an investigation on the effects of acute psychosocial stress on task performance. Particularly, Chapter 6 demonstrated that stress impaired the rate of saccadic adaptation, and that this impairment was associated with the stress-related endocrine response. The study presented in Chapter 7 showed no effect of psychosocial stress on postural balance control. Finally, Chapter 8 explored the effects of non-invasive cerebellar stimulation on saccadic adaptation and cortisol output, revealing that a decrease in cerebellar excitability yielded adaptation rates that were similar to those observed after stress. These findings suggest that psychosocial stress impairs error-driven feedforward computations specifically, via glucocorticoid signalling, thus contributing to the current neurobiological models of stress.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available