Dr. Johnson is most well-known for his work on the molecular, cellular and behavioral effects of phencyclidine (PCP, “angel dust”) in young postnatal rats. This work focused largely on PCP’s interactions with the N-methyl-D-aspartate (NMDA) glutamate receptor subtype and has been the cornerstone of his research career. Following several studies on the behavioral effects of PCP in adult rats, he became interested the hypothesis that young, immature animals could be particularly vulnerable to the effects of drugs like cocaine, and particularly, PCP. This work was largely carried out in perinatal rats that were treated with PCP on postnatal (PN) days 7, 9, and 11. This treatment regimen caused the apoptotic, caspase-3-dependent death of a number of neurons (especially parvalbumin containing neurons) in the prefrontal cortex, thalamus, hippocampus, subiculum and striatum. This was associated with significant schizophrenia-like behavioral changes later in life such as behavioral sensitization to a small dose of PCP (on PN42), a loss of pre-pulse inhibition of acoustic startle on PN24-25, as well as a deficit in acquisition of delayed spatial alternation task (thought to be dependent on short-term working memory and known to be deficient in schizophrenia). The mechanism by which PCP caused neuronal death was shown to involve both the PI-3 kinase/Akt/GSK-3β and MEK/ERK pathways, which could be ameliorated by lithium and BDNF (in vitro). Later, we were able to demonstrate that activation of dopamine D1 receptors could compensate for the effect of PCP by activating both PKA, which increased NR1 trafficking to the synapse, as well as FYN kinases, which in turn activated Src kinases that enhanced NR2B trafficking into the synapse. These effects increased synaptic strength and cell survival through the PI3K/Akt/GSK-3B cell survival pathway, suggesting that D1 receptor activation could be useful in treating psychoses such as schizophrenia which is now most typically treated with D2 receptor antagonists.