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The above streams of research have recently converged, allowing us to investigate how early life experiences, temperamental traits, and neurobiology combine in health, disease, and recovery.
Childhood trauma is the prototypical transdiagnostic risk factor for near all psychiatric problems. We have been studying these effects for over 30 years, first in isolation from other influences, more recently in combination with additional risk factors.
This is a relatively new area for us. However, recent collaborations with Cecilia Flores (McGill and Douglas Institute) allowed us to identify large effects of a single gene mutation on brain development and behavior. Subsequent collaborations with Jacob Hooker (Harvard) have permitted the study of epigenetic processes in human brain, using the first PET tracer for HDACs.
Through collaborations with colleagues throughout Quebec (Ashley Wazana, Michael Meaney, Jean Séguin, Natalie Castellanos-Ryan, Michel Boivin, Patricia Conrod), we studying developmental trajectories (biological and behavioral) to diverse, commonly comorbid conditions (e.g., mood, anxiety and substance use disorders) and psychoses.
We use positron emission tomography (PET) to measure epigenetic processes and dopamine, glutamate and serotonin system features in diverse populations. This is complemented by magnetic resonance imaging to measure both structural features (morphology, anatomical connectivity, etc) and neurotransmitter-independent brain activations.
We have documented conditioned and sensitized dopamine responses in humans and how these effects evolve following progressively greater substance use.
In a PET study of youth who have been followed from birth (n=52), a combination of early life adversity, high externalizing behavioral traits, and low midbrain dopamine autoreceptor availability predicted, with over 90% accuracy, lifetime histories of commonly comorbid early onset disorders. CIHR funding has been obtained to conduct follow-up PET scans and roughly double the sample size.
A series of PET and dopamine synthesis inhibition studies has allowed us to test both correlational and causal hypotheses in humans. Together, these studies addressed core issues in psychology, behavioral neurobiology, and addictions, indicating that (a) pleasure is not required for changes in motivational states, (b) the neurobiology is not the same, and (c) since dopamine affects motivation to seek drug reward but is not closely related to drug-induced pleasure, addiction treatments will likely benefit from a dopamine component and yet we now understand why this has not proven sufficient.
Knowledge translation has been a part of our work for over a decade. By taking the time to integrate the requisite knowledge, we have been able to present social implications of behavioral neuroscience research to non-public policy specialists. Bridging these disciplinary gaps has become an unexpected pleasure.
