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Conditioned taste aversion (CTA) is a unique form of associative learning in which an animal learns to pair a particular flavor (either neutral or palatable) with internal malaise (Garcia et al. 1955; see also Yamamoto & Fujimoto 1991). The resulting behavioral response includes avoidance and rejection of the now aversive flavor during future encounters. What separates this form of learning from other classical conditioning paradigms is the length of time allowed between the pairing of the conditioned stimulus (CS = novel taste exposure) and unconditioned stimulus (US = mild nausea induced by LiCl injection, i.p.), on the order of several hours, with little effect on CTA learning (Garcia et al. 1974). Compare this to other forms of learning in which the pairing requires less than a 1-2 sec delay. This special feature of CTA learning is intuitive when one considers the need for an animal to delay making a judgment on the hedonic value of a novel taste until the visceral consequences of its ingestion can be assessed. The unique features of CTA learning grant researchers the opportunity to directly observe and manipulate each phase of the conditioning paradigm in the hopes of elucidating the learning-related changes in neuronal activity. It is in this spirit, I have chosen to focus my graduate research studies on the neural mechanisms involved in CTA. Using chronically implanted extracellular recording electrodes, I am able to record the activity of an ensemble of isolated neurons in the rat amygdala (AM) and gustatory center of the insular cortex (GC) during all phases of CTA training and testing. The benefit of this method is the ability to isolate several neurons in each area simultaneously and chronically, and record spike activity and local field potentials (LFP) at any time for a time period of up to two weeks. In this way, changes in neuronal activity in both AM and GC can be monitored throughout the presentation of the novel taste and LiCl-induced internal malaise as well as during subsequent taste exposure. The hypothesis that I am testing is that a conditioned aversion to a previously palatable tastant involves the formation of emergent connections between the AM and GC during the period of internal malaise and that these connections persist throughout future tastant exposures. By employing a series of statistical analyses on the temporal dynamics of stimulus-response spike activity, it is possible to assess the changes in activity in AM and GC. Among these changes, I will test for the presence of direct or indirect (monosynaptic of polysynaptic) connections emergent with learning, responsible for the linking of 'sucrose' with 'aversive'. Possible future directions include a pharmacological blockade of some aspect of learning or normal neuronal functioning (e.g., NMDA-receptor antagonist, muscimol, lesioning) in either GC or AM to observe the effects on CTA learning along with neuronal changes associated with learning. It is my hope that these studies will broaden our understanding of this peculiar form of learning, learning and memory in general, and the temporal dynamics of learning-related changes in neuronal activity. |
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Bibliography:
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 Brandeis University |
 Brandeis University Dept. of Psychology |
 Volen Center for Complex Systems |
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