Browsing by Author "Gabriele, Amanda"
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Item Multiple memory systems and extinction(Texas A&M University, 2005-08-29) Gabriele, AmandaSeveral lines of evidence suggest that initial acquisition of learned behavior involves multiple memory systems. In particular, lesions of the hippocampus impair the acquisition of cognitive or relational memory, but do not impair the acquisition of stimulus-response habits. Extinction behavior also involves new learning, and therefore it is possible that multiple forms of memory may also underlie extinction. We examined this hypothesis by training rats in a task in which extinction behavior could putatively be acquired by either a cognitive or habit memory system. Adult male Long-Evans rats were initially trained to run in a straight alley maze for food reward. Following training they were placed into one of two extinction conditions. In one condition rats were allowed to run to an empty goal box (i.e. response extinction). In a second condition rats were placed into an empty goal box without making a running response (i.e. latent or non-response extinction). Prior to each daily session of extinction training, rats received intra-hippocampal infusions of either the local anesthetic bupivacaine (0.75% solution/0.5 ul), or saline. Rats receiving saline infusions displayed extinction behavior in both the response and non-response conditions. In contrast, rats receiving intra-hippocampal infusions ofbupivacaine extinguished normally in the response condition, but did not display nonresponse extinction. This latent extinction effect was enhanced by decreasing the amount of time between the last extinction trial and the probe trial. Additionally, administering extinction training and probe trials in different contexts did not appear to prevent latent extinction, however large variability may be masking this effect. The new context administered during extinction prevented latent extinction in some animals, but not others. These findings suggest that, similar to initial acquisition, the learning that occurs during extinction also involves multiple memory systems. Specifically, the hippocampus may selectively mediate extinction under conditions in which new stimulus-response learning is prevented.Item Multiple memory systems and extinction: the neurobiological basis of latent extinction(2009-05-15) Gabriele, AmandaUnderstanding the neural mechanisms underlying the extinction of maladaptive behaviors has become increasingly relevant. Extinction, or the reduction of a response due to lack of reinforcement, is believed to be ?new learning.? Most extinction paradigms involve the performance of the previously reinforced response in the absence of reinforcement in order for extinction to occur. Conversely, latent extinction is a cognitive form of learning in which the previously rewarded response is not made during extinction training. However, until now the neurobiological basis of latent extinction has remained unknown. This dissertation has three aims to examine the neurobiological basis of latent extinction. Previous research has shown latent extinction to be impaired following hippocampal inactivation and the goal of Aim 1 was to examine other neural systems potentially involved in latent extinction through examination of brain structures such as the dorsal striatum, medial prefrontal cortex, and basolateral amygdala. Additionally, the neurochemical basis of latent extinction is unidentified; therefore Aim 2 addressed this question, specifically investigating the glutamatergic system through both NMDA receptor agonism and antagonism. Finally, understanding latent extinction may be useful for the extinction of drug addiction. Aim 3 was to examine some clinical implications for the extinction of drug addiction utilizing latent extinction following maze running for an oral cocaine reward. Reversible neural inactivation studies using the sodium channel blocker bupivacaine demonstrated a selective impairment of response extinction following dorsal striatum inactivation, but no effect on either latent or response extinction following medial prefrontal cortex or basolateral amygdala inactivation. These results, coupled with previous data from our lab demonstrate a double dissociation for extinction behavior. Further, peripheral NMDA receptor agonism with D-cyloserine enhances latent extinction and intra-hippocampal NMDA receptor antagonism with AP5 impairs latent extinction, identifying a role for the glutamatergic system in latent extinction. Finally, oral cocaine administration during acquisition selectively impairs latent extinction indicating that drug use affects the relive use of multiple memory systems during extinction. Overall, the multiple memory systems theory and latent extinction provide a framework with which to further understand the neural mechanisms of extinction behavior.