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• W2149277263 abstract "It has been suggested that post-traumatic stress disorder sufferers (PTSD) fail to extinguish the conditioned fear response to the traumatic stimuli which demonstrates the usefulness of an animal model for understanding human PTSD (Milad, 2006; Rauch, 2006). The N-methly-D-aspartate (NMDA) system plays a critical role in the extinction of a fear response. In fact, NMDA antagonism has produced dose dependent blockages of extinction (Falls et al., 1992) while ~-cylcoSerine (DCS), and NMDA agonist, has shown to be effective in facilitating the extinction process (Walker et al., 2002). Experiment 1 did not find results similar to those found in the literature. Interestingly, DCS actually facilitated an augmented fear response with 24 hour, 7 day, and 30 delay periods between extinction sessions. Experiment 2 also did not find that DCS aids the extinction learning process but was able to eliminate the augmentation of the fear response found in experiment 1 by extinguishing animals to a criterion level before DCS manipulation. The lack of statistical power may have been the largest hindrance on the absence of effects seen in experiment 2. However, together these experiments show that an initial learning must take place in order for DCS to be effective. Ultimately, if there is certain sensitive population with which DCS can be efficacious, then an animal model of PTSD which utilizes DCS may be of limited value. In turn, DCS use in humans may only render a response in those that exhibit an initial reduction in fear. Otherwise, DCS may actually serve to enhance their fear response. DCS and Fear Extinction The extended effects of D-cycloserine treatment on fear extinction in rats. Animal research investigating fear, anxiety, and disorders related to such involves animal models and typically uses Pavlovian fear conditioning paradigms in which a conditioned stimulus (CS), such as a light or tone, is paired with an aversive event (shock), or unconditioned stimulus (US). Throughout multiple trials of these pairings, the animal becomes conditioned to fear the CS usually causing increased anxiety and a conditioned response (CR). For example, rats generally exhibit this fear by freezing, a species specific behavior that is characterized by total lack of movement save for respiration. Later, in the process of extinction, the CS is presented to the animal in the absence of the US. The CR associated with the CS begins to diminish over trials, seemingly because this response is no longer adaptive. The conditioned response is thus used as an indirect measure of fear and the memory for the CS-US relationship. Although it is generally accepted that it is not that the fear has been forgotten, but rather the new association of the CS coupled with the absence of the US forms a new memory which then competes with the original association for fear expression (Milad et al., 2006). Like experimental animals, humans may also employ the same processes to acquire and get rid of a fear response. It has been suggested that post-traumatic stress disorder sufferers (PTSD), however, fail to extinguish the conditioned fear response to the traumatic stimuli which demonstrates the usefulness of this exemplar for understanding human PTSD (Milad, 2006; Rauch, 2006). Presently, therapies for PTSD and phobias include an exposure-based program, which closely resembles the extinction process used in animals (Foa, 2000; Rothbaum & DCS and Fear Extinction Davis, 2003). Patients are consistently presented with the stimuli once found to be traumatic without any negative or aversive consequences in hopes that their fear response will diminish over time. Nevertheless, this type of therapy has severe limitations because disordered patients typically do not respond normally over time to this form of extinction training in that the anxiety response habitually returns and does not usually transfer outside the experiment to real world anxiety inducing situations (Foa, 2000; van Minnen et al., 2002). Thus, PTSD is typically believed to support the idea of extinction failure. Therefore, while the clinical applications of extinction training seems obvious, a clearer understanding of the neural mechanisms involved in extinction could generate improved biological approaches to treat fear and anxiety related disorders, like PTSD. The Role of the Amygdala The amygdala has long been implicated in the expression of fear and anxiety. The amygdala receives input from several sensory regions and mediates the expression of fear as well as anxiety, among other emotional responses (Fendt & Fanselow, 1999) and so is essential to formation and expression of aversive memories (Davis et al., 2005; Aggleton, 2000). Additionally, the central nucleus of the amygdala may mediate several different components of the fear response because it is this area that first projects to cortical and brain stem areas that control these responses (Kapp, Silvestri, & Guarraci, 1998). Barad (2006) also reviews literature indicating that the basolateral amygdala (BLA) is central to fear conditioning as well. The information from aversive stimuli is first processed in the BLA and is then forwarded to the central nucleus resulting in the" @default.
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• W2149277263 title "An Examination of the Extended Effec ts of D- Cycloserine Treatment on Fear Extinction in Rats" @default.
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