<p> Contextual fear conditioning involves pairing a novel context (conditioned stimulus) with several footshocks (unconditioned stimulus) that serve to condition fear to that context. As the retention interval between training and testing increases context specificity is lost. In other words, the fear memory is no longer precise or context-specific, but has generalized to novel contexts at remote time points. In an attempt to investigate the neural pattern of an imprecise contextual memory trace as a function of time, we used fluorescent in situ hybridization to for Arc mRNA as a measure of neuronal activation following expression of a precise vs. imprecise context fear memory. Expression of a contextually precise memory involved increased Arc mRNA expression in both the dorsal and ventral CA1 regions of the hippocampus as well as the ACC and IL. Expression of a contextually imprecise fear memory involved Arc mRNA expression in the ventral CA1, ACC, IL, and the PL suggesting that both the hippocampus and prefrontal cortex are involved in the expression of a remote contextually imprecise memory. Further, inactivation of the ACC at remote time points returned the context memory to a precise state, but had no effect on memory for the training context. Taken together, these data suggest that as a context fear memory ages, both the hippocampus and prefrontal cortex interact in the expression of the memory trace resulting in the loss of precision. Preventing this interaction through inactivation of the ACC allows the hippocampus to express the contextually precise memory. In addition to the systems investigation of fear generalization, we also investigated a potential synaptic mechanism of the phenomenon. Specifically, we discovered that mice lacking a GABAB1 receptor subtype, GABAB1a, exhibit a loss of context discrimination compared to wild-type animals. Animals lacking GABAB1a receptors showed a significant, but not complete loss of context specificity 24 hours post-training. GABAB1a knock out mice exhibited a complete loss of context discrimination by 5 days post-training. However, knock out mice exhibited normal context discrimination immediately following training, suggesting that GABAB1A receptors are necessary for the retention, but not acquisition, of context discrimination. Our results indicate that presynaptic inhibition is required for the maintenance of context. </p>

In order to clarify the relationship between anxiety vulnerability and clinical anxiety, information-processing models have been employed to examine the cognitive biases of anxious individuals for threat-related information. At the core of these models are research findings indicating that anxiety-linked attentional biases render high trait anxious individuals disproportionately vulnerable to the effects of stress. The current research, following the model of Williams, Watts, MacLeod, and Matthews (1988), tested the hypothesis that attention to threat-related information is due to the interaction of trait anxiety and state anxiety. / Five comparable studies employed emotional Stroop and probe-detection paradigms to assess the attentional biases of high and low trait anxious individuals to threat-related words in response to elevations of stress. Four of the studies assessed the preconscious and conscious attentional biases of adults and one study investigated the attentional biases of children. This focus allowed developmental comparisons that had not been undertaken previously. The studies were comparable to each other and to previous research. The studies sought to clarify the effects of different forms of stress on the anxiety-linked attentional biases and to assess the effects of these stressors on domain-specific stimuli. The hypotheses were that, in response to elevations in state anxiety, high trait anxious individuals show increased attention to threat and low trait anxious individuals show avoidance of threat. It was expected that these threat-related attentional biases are identified at both preconscious and conscious levels of processing, and more when the stimuli are related to the individuals’ domain of concern. / Contrary to expectations, only one study found the predicted pattern and this result occurred at a conscious level of processing. In addition to the lack of support for the hypotheses, a counter-intuitive alternative pattern that was the converse of predictions was identified in four of the five studies. In this pattern, in response to elevated stress, there was a trend for high trait anxious individuals to show decreased attention to threat and low trait anxious individuals to show increased attention to threat. The pattern was identified, in various studies, at conscious and preconscious levels of processing, and more in response to domain-specific stimuli. Adults and children showed similar levels and types of attentional biases. / The results of the current studies show some convergence with previous research. The findings are discussed in the context of a proposed model that incorporated aspects of Williams et al’s theories (1988; Williams, Watts, MacLeod, & Mathews, 1977) and Mogg and Bradley’s (1988) theory. This model suggests that high and low trait anxious individuals’ patterns of threat-related attentional biases vary according to their different levels of reactivity to stress, which affects their threat threshold. Due to differences in this threat threshold, high and low trait anxious individuals show divergent attentional responses under the same level of external stress. The model incorporates the avoidance effects identified in previous research and theory. This model may explain both the current counter-intuitive findings and past inconsistencies in the literature. It may also clarify how individuals with different levels of anxiety vulnerability show divergent attentional responses to stress elevations. It is suggested that inclusion of the notion of subjective stimulus threat value into the cognitive processing paradigm may clarify some of the unresolved issues raised in this research.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 1999. / Source: Dissertation Abstracts International, Volume: 60-06, Section: B, page: 2959. Adviser: Stephen Hibbard.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 1999. / Source: Dissertation Abstracts International, Volume: 60-11, Section: B, page: 5837. Adviser: William J. Froming.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 2000. / Source: Dissertation Abstracts International, Volume: 61-03, Section: B, page: 1663. Adviser: William J. Froming.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 2000. / Source: Dissertation Abstracts International, Volume: 61-07, Section: B, page: 3874. Chair: William J. Froming.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 2000. / Source: Dissertation Abstracts International, Volume: 61-08, Section: B, page: 4439. Adviser: William Nasby.

Thesis (Ph. D.)--Pacific Graduate School of Psychology, 2002. / Source: Dissertation Abstracts International, Volume: 62-12, Section: B, page: 6015. Adviser: Larry W. Thompson.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 2002. / Source: Dissertation Abstracts International, Volume: 63-08, Section: B, page: 3936. Adviser: Amy M. Wisniewski.

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 2003. / Source: Dissertation Abstracts International, Volume: 64-06, Section: B, page: 2931. Adviser: Amy Wisniewski.