Education:
B.S., Biology, Stephen F. Austin University (1967)
Ph.D., Biochemistry, University of Houston (1969-1974)
Postdoctoral Fellowship, Pharmacology, Medical College of Virginia (1975-1977) 

Research Interests:
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. 

Selected Publications: (from 161 peer-reviewed articles, 7483 Google Scholar citations, h-index-47, i10 index-144)  

1. Wang, C.Z. and Johnson, K.M. The role of caspase-3 activation in phencyclidine-induced neuronal death in postnatal rats. Neuropsychopharmacology 32: 1178-1194, 2007. PMID 16985504  
2. Lei, G., Xia, Y. and Johnson, K.M. The role of Akt-GSK-3β signaling and synaptic strength in phencyclidine-inducedneurodegeneration.Neuropsychopharmacology33:1343-1353, 2008. PMID 17637606  
3. Wang, C.Z., Yang, S.F., Xia, Y. and Johnson, K.M. Postnatal phencyclidine administration selectively reduces adult cortical parvalbumin-containing interneurons. Neuropsychopharmacology 33: 2442–2455, 2008. PMID 18059437  
4. Anastasio, N.C. and Johnson, K.M. Differential regulation of the N-methyl-D-aspartate receptor by acute and subchronic phencyclidine administration in the developing rat. J. Neurochem. 104:1210-1218, 2008. PMID 17995927  
5. Anastasio, N.C. and Johnson, K.M. Atypical antischizophrenic drugs prevent changes in cortical N-methyl-D-aspartate receptors and behavior following sub-chronic phencyclidine administration in developing rat pups. Pharmacology, Biochemistry and Behavior 90:569-577, 2008. PMID 18544461  
6. Xia Y, Wang CZ, Liu J, Anastasio NC, Johnson KM. Lithium protection of phencyclidine-induced neurotoxicity in developing brain: The role PI-3K/Akt and MEK/ERK signaling pathways. J Pharmacol Exper Therap 326:838-848, 2008. PMID 18544676 PMCID PMC2561310  
7. Lei, G., Anastasio, NC, Fu, Y, Neugebauer, V and Johnson, KM. Activation of dopamine D1 receptors blocks phencyclidine neurotoxicity by enhancing N-methyl-D-aspartate receptor mediated synaptic strength. J. Neurochemistry 109: 1017-1030, 2009. PMID 19519774 PMCID PMC2709756  
8. Xia, Y, Wang, CZ, Liu, J, Anastasio, NC, Johnson, KM. Brain-derived neurotrophic factor prevents phencyclidine-induced apoptosis in developing brain by parallel activation of both the ERK and PI-3K/Akt pathways. Neuropharmacology 58: 330-336, 2010. PMID 19887077 PMCID PMC2813345  
9. Chen, H., Wang, CZ, Cheng Z., Ding, C., Wild, C., Copits, B., Swanson, G.T., Johnson, K.M. and Zhou, J. A combined bioinformatics and chemoinformatics approach for developing asymmetric bivalent AMPA receptor positive allosteric modulators as neuroprotective gents. ChemMedChem 8:226-230, 2013. PMID: 23281122. [Associated patent: J. Zhou, H. Chen, K.M. Johnson, C.Z. Wang, Bivalent AMPA Receptor Positive Allosteric Modulators. US 61/605,631, 03/01/2012]  
10. Timpe, J., Wang, CZ and Johnson, KM. AMPA receptor activation protects against phencyclidine-induced neurotoxicity via activation of voltage gated calcium channels. J Neurosci Res. 92: 1785-1791, 2014. PMID: 24995437