Dr. Darragh P. Devine, Ph.D.

Professor and Director
Behavioral and Cognitive Neuroscience
Department of Psychology & Neuroscience

Contact Information

Email: dpdevine@ufl.edu
Phone: (352) 273-2174
Office: 324 Psychology Building

Mailing address:
University of Florida
PO Box 112250
Gainesville, FL 32611

Research Statement

NEUROBIOLOGY OF SELF-INJURIOUS BEHAVIOUR: Self-injurious behaviour is arguably the most debilitating of all the pathological characteristics that are observed in patients with neurodevelopmental disorders. Typically, afflicted patients exhibit head-banging, self-biting, and/or self-punching behaviours. These behaviours carry the risk of extreme physical harm, and they interfere with all normal functions of daily living, including educational and socializing activities. In addition, self-injury is destructive for families of afflicted patients, and the cost of specialized care is over $3 billion annually in the United States. Self-injurious behaviour is particularly prevalent in autism spectrum disorders, Lesch-Nyhan syndrome, Prader-Willi syndrome, and other genetically-determined disorders. However, the incidence and severity is highly variable within most of these diagnostic groups.

Most investigations of self-injury focus upon psychosocial aspects of the behavior disorder (e.g. functional analysis and intervention to address reinforcing social interactions that maintain these behaviors). This approach has yielded treatment programs that are partially effective for many patients, and behavior therapy is clearly the treatment of choice. However, social reinforcement does not contribute to the maintenance of SIB in over 30% of cases, and many self-injurers (e.g. Lesch-Nyhan syndrome) are particularly resistant to behavioral interventions.

We have focused our research efforts upon identification of neuropathological variables that may underlie shared vulnerability for etiology of self-injury across neurodevelopmental disorders. One important clue is that self-injurious behaviour is highly prevalent in genetic disorders where ongoing distress, pathological irritability, and abnormal physiological stress responses are prominent features. Additional clues come from clinical trials of pharmacological interventions, from-post mortem neurochemical analyses, and from studies in animal models. The convergent evidence from these three lines of research indicates that dopaminergic insufficiency is a common element in vulnerability for self-injury. A prevailing (and decades old) interpretation is that the dopaminergic deficits cause postsynaptic supersensitivity. However, biochemical investigations of this putative supersensitivity are lacking. Therefore, our understanding of the biological basis of self-injurious behaviour lags far behind our understanding of virtually every other major neuropsychiatric dysfunction.

We are studying the neurobiological basis of vulnerability for self-injury in an animal model. In our model, rats exhibit self-biting behaviour after 4-5 days of treatment with pemoline (a monoamine uptake blocker). We have refined the model, improved behavioral measures, and identified multiple lines of congruence between clinical and pemoline-induced self-injury. Most importantly, individual rats differ in vulnerability, and this is based upon innate stress-responsive phenotypes. In addition, dopamine stores are depleted during the induction of self-injurious behaviour, and exposure to stress exacerbates the symptoms of self-injury. All these characteristics are redolent of findings in human self-injurers. We are currently investigating biochemical measures of neuronal sensitivity that may differentiate vulnerable from resistant rats in the pemoline model. These studies will promote our understanding of the brain mechanisms that underlie the etiology of this devastating behavioural pathology.

TRAINING OPPORTUNITIES: Students in my laboratory have extensive opportunities to participate in the ongoing research program. They routinely learn and practice state-of-the-art methods in analysis of pharmacologically-induced and environmentally-induced alterations in behaviour. This is combined with assays of concomitant changes in neurochemistry, hormonal responses, and gene regulation. A major goal of training in my laboratory is to foster critical thinking as it relates to important issues in behavioural and molecular neuroscience.