Your Brain Cells On Drugs-Measuring Plasticity
Panel 1 : Shows a photo of a brain cell and its dendrites from the nucleus accumbens from a subject exposed to drugs of abuse.
Panel 2 : This is a camera lucida representation of the brain cell from Panel 1.
Panel 3 : This cameral lucida representation of the same brain cell provides an analytical approach toward neural plasticity. This approach measures the number of spines and the complexity of dendritic branching pattern.
Non-medical use and abuse of prescription opiates is rising so that its prevalence is greater than that of heroin or cocaine abuse. In military and VA settings, soldiers and Veterans face acute or chronic pain that is managed by opiate narcotics and misuse of these agents is widely reported. Behavioral therapies and opiate substitution treatment for opiate addiction are time-intensive approaches that are incompletely effective and often inaccessible. During drug-taking, individuals are exposed to environmental cues or contexts where drugs of abuse are administered. The development of strong drug cue or contextual preferences accelerates the transition from intermittent drug use to drug addiction. Future exposure to these same cues elicits conditioned seeking behaviors and relapse via associative learning processes. Our research examines the neurobiological mechanisms and treatment approaches to enhance the extinction of these conditioned drug responses. Our preclinical research examines neuroplasticity and mechanisms of conditioned opiate reward and its extinction and tests novel pharmacological and behavioral extinction learning approaches in C57BL/6 mice.
Post-Traumatic Stress Disorder (PTSD)
Veterans are returning from deployment with increased rates of psychiatric symptoms including PTSD. This is not surprising, given that combat intensity elevates the risk of both physical and psychological injuries. Fear acquisition and extinction learning in rodent models can improve our understanding of post-traumatic stress disorder (PTSD). Such learning may be produced by changes in dendritic spine morphology and connectivity in multiple brain regions including prefrontal cortex, hippocampus, and basolateral amygdala. Our preclinical research examines neuroplasticity and mechanisms of fear conditioning and its extinction and tests novel pharmacological and behavioral extinction learning approaches in C57BL/6 mice.