Dr. Johnson's research interests are largely in the area of drug mechanisms, particularly drugs of abuse, and animal models of psychiatric disease. He has a long-standing interest in neurotransmitter receptor function and the mechanisms by which drugs of abuse alter neurotransmitter signaling. In an attempt to discover therapeutic agents for cocaine abuse his lab collaborated with organic chemists and discovered several chemical scaffolds capable of inhibiting cocaine binding with only minimal effects on the uptake of neurotransmitters which were inhibited by cocaine. His major research effort was focused on determining the mechanism by which phencyclidine (PCP) caused psychosis, and how this information might eventually be used to understand how to diminish the symptoms of schizophrenia. This work focused on the long-lasting schizophrenia-like effects of phencyclidine treatment in young rat pups and how this might be used to understanding the cellular/biochemical mechanisms underlying the enduring schizophrenia-like behavioral effects observed following perinatal phencyclidine (PCP) administration. Additional experiments showed that PCP-induced blockade of calcium conducting NMDA receptors resulted in alterations in ERK1/2 and PI3K signaling mechanisms related to BDNF and other important pathways in perinatal rats. Most recently the lab demonstrated that activation of AMPA receptors could prevent PCP-induced neuronal death and that this effect was dependent on depolarization- activation of L-type calcium channels and TrkB, a major BDNF signaling partner. These data suggest that activation of TrkB via calcium influx though these channels may have therapeutic potential.
Publications/Creative Works
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Affiliations
Research Consortia
Gulf Coast Cluster for Translational Addiction Science
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