Research in our laboratory is currently focused on two major projects. One project deals with analysis of the physiological and behavioural consequences of acute and chronic stress exposure. We are currently examining the neurobiology of stress using highly emotional (as opposed to physiological) stressors, as we believe that this approach models the type of stress exposure that humans routinely experience. Human emotional stress exposure appears to be very important in the onset and maintenance of a variety of psychopathological conditions. Accordingly we are examining individual differences in vulnerability to stress-induced psychopathology, neuroadaptations that occur during chronic stress exposure, and the specific neurotransmitter systems and hormonal systems that participate in stress-induced psychopathology. We coordinate all our studies with examinations of behavioural concomitants of the stress exposure, and we focus largely on evaluation of anxiety-related behaviours.
The other major focus of my laboratory is the neurobiological basis of self-injurious behaviour. Self-injury is a devastating behavioural disturbance that is expressed by individuals with autism, Lesch-Nyhan syndrome, intellectual handicaps, and other conditions. The disorder is poorly understood at present. We have identified specific variables that confer increased or diminished vulnerability to self-injury, and we are examining the neurobiological concomitants of this vulnerability to self-injure.
In each of these research endeavours, we combine a variety of behavioural, cellular and molecular analyses to uncover the neurobiological basis of the observed responses.
I have recently completed a study which involved the effects of cortically derived stress on algesia (sensitivity to pain.) Rats were trained in a thermal preferece test in which they learned to move between a hot and cold platform. Temperatures were adjusted such as they spent 50% of the time in each compartment during a 15 minute trial. Animals were then stressed usign the social defeat model, which has been shown by our lab to cause hormonal disregulation and induce depressive like behavior. Changes in thermal compartment preference quantitatively account for changes in thermal pain perception. A sperate trial was run in which valium was administered prior to stress. Results from these trials were similar to baseline indicating that the valium inhibited those effects induced by stress. A more detailed description and analysis can be viewed here, which were presented at UF's annual pscychology research forum.