Background

Most of my interest in psychology is aimed at furthering our understanding of the biology of psychiatric disorders that may lead to more effective treatments and preventive strategies. For example, our understanding of the mechanism of action of selective serotonin reuptake inhibitors in depression is still minimal, and the current monoamine hypothesis of depression is being regularly challenged by new research. While it was previously believed that the mechanism was the increase in synaptic serotonin levels, the fact that SSRIs often take weeks or months to take effect brought into doubt that hypothesis, since intra-synaptic serotonin levels are increased weeks before the antidepressant activity takes effect. Thus, it has been postulated that the effect of our current pharmacotherapy may be from a "cascade" of reactions that the drug initiates, leading to adaptive changes in the glutamate and CRF systems, for example.

In recent years, new theories surrounding depression etiology and treatment have emerged. Several studies have implicated the glutamate and CRF systems in the end effect of the cascade described above. Ketamine, an NMDA-receptor antagonist, has been shown to be effective against depression in several preclinical trials. Additionally, depressed patients also have a chronically activated stress response which leads to cellular death, especially in the hippocampus. Hippocampal neurogenesis has been found as a result of SSRI treatment and is one possible explanation of their mechanism of action.

Research Interests

I am interested in the role of the glutamate and CRF receptor systems in depression, and increasing our understanding of the role that those systems plays in depression neuropathology and eventual treatment. I would like to better understand how current treatments work in relation to these new hypotheses regarding the mechanism of action of these treatments, and how we can learn more about these systems to develop treatments with faster onset and higher efficacy. How can we apply our knowledge of the biological mechanisms of depression and other disorders to prevention as well as treatment? Within a diathesis-stress framework and our new biological theories, what biological and environmental factors interact to form psychopathology?

I am also interested in the role of other systems in mood and anxiety disorders, such as the amygdala in anxiety, the caudate nucleus in OCD, and the brain systems involved in criminal behavior (neurocriminology). Other research interests include novel psychopharmacological models for mood and anxiety disorders; the role of the endocannabinoid system in mood and motivation; and the psychopharmacology of drugs of abuse.

Unless otherwise stated, content by Greg Hard is licensed via the Creative Commons Attribution-Share Alike United States License

Publications

None Currently Available

Research Interests

|  Neurobiology of Mood Disorders
|  Affective Neuroscience
|  Motivational and Fear Systems
|  Neurocriminology and Forensic Psychology
|  Psychopharmacology