[Truncated abstract] Over the past several decades substantial research has been conducted investigating the association between attentional bias to emotionally threatening material and anxiety. Tasks such as the emotional Stroop, the dichotic listening task and the visual probe task have been used to document this association, with the visual probe task providing the most direct means of assessing this bias. That this association exists stands beyond contention, however relatively little research has been conducted directly examining the causal nature of this relationship. By using predictive and recovery approaches it is possible to determine how attentional bias and anxiety co vary but not the exact causal nature of this relationship. However, when the visual probe methodology is used attentional bias to threat can be directly manipulated and as such it is possible to determine if attentional bias to threat causally underpins the development and maintenance of anxiety. The purpose of the current research was to deliver an extended attentional training task to anxious individuals by capitalising upon the ability to directly manipulate attentional bias using the visual probe task methodology and assessing the possible therapeutic benefits of such an approach. ...Nevertheless these results provided support for the validity of the causal hypothesis and the technological difficulties associated with administering the task online were ameliorated. Due to the fact that characteristics of both situational and dispositional anxiety are present in a clinical population a revised version of the attentional training task was administered to two groups of non-clinically anxious individuals to determine the impact that avoid threat attentional training has on each of these types of anxiety. High trait anxious students and pregnant women were chosen for this purpose but due to substantial attrition these two experiments failed to provide sufficient evidence to evaluate the causal hypothesis. Two main reasons for this attrition were identified, the motivation of participants and the procedures that were in place to monitor their progress. To ensure that attrition would not compromise future experiments a series of modifications were made and the attentional training program was then readministered to a sample of individuals characterised by dispositional or situational anxiety. A group of self labelled worriers and a sample of Immigrating Singaporean students respectively, were chosen for this purpose. There was no significant influence of avoid threat training on attentional bias for the self labelled worriers, nor any evidence of an attenuation of emotional vulnerability. For the Immigrating Singaporean students, however; there was evidence of a significant reversal of attentional bias to threat post attentional training compared to the control group and a corresponding attenuation of emotional vulnerability and a trend towards a significant attenuation of emotional reactivity. The implications for the causal hypothesis and the therapeutic applicability are discussed as well as several avenues for future research.

Indiana University-Purdue University Indianapolis (IUPUI) / Anxiety disorders are estimated to impact 1 in 4 individuals within their lifetime. For some individuals, repeated episodes of the stress response leads to pathological anxiety and depression. The stress response is linked to increased levels of corticotropin-releasing factor (CRF) in the basolateral nucleus of the amygdala (BLA), a putative site for regulating anxiety and associative processes related to aversive emotional memories, and activation of CRF receptors in the BLA of rats produces anxiety-like behavior. Mimicking repeated episodes of the stress response, sub-anxiogenic doses of urocortin 1 (Ucn1), a CRF receptor agonist, are microinjected into the BLA of rats for five consecutive days, a procedure called priming. This results in 1) behavioral sensitization, such that a previously non-efficacious dose of Ucn1 will elicit anxiety-like response after the 3rd injection and 2) the development of a persistent anxiety-like phenotype that lasts at least five weeks after the last injection without any further treatment. Therefore, the purpose of this thesis was to identify mechanisms involved in the Ucn1-priming-induced anxiogenesis. The first a set of experiments revealed that the anxiety-like behavior was not due to aversive conditioning to the context or partner cues of the testing environment. Next, Ucn1-priming-induced gene expression changes in the BLA were identified: mRNA expression for Sst2, Sst4, Chrna4, Chrma4, and Gabrr1 was significantly reduced in Ucn1-primed compared to Vehicle-primed rats. Of these, Sst2 emerged as the primary receptor of interest. Subsequent studies found that antagonizing the Sstr2 resulted in anxiety-like behavior and activation of Sstr2 blocked acute Ucn1-induced anxiety-like responses. Furthermore, pretreatment with a Sstr2 agonist delayed the behavioral sensitization observed in Ucn1-induced priming but did not stop the development of persistent anxiety-like behavior or the Ucn1-priming-induced decrease in the Sstr2 mRNA. These results suggest that the decrease in Sstr2 mRNA is associated with the expression of persistent anxiety-like behavior but dissociated from the mechanisms causing the behavioral sensitization. Pharmacological studies confirmed that a reduced Sstr2 mediated effect in the BLA is likely to play a role in persistent anxiety and should be investigated further.