Ronald L. Davis, Ph.D.
Professor and Chair
Adjunct Professor - Department of Molecular and Cellular Biology and Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston TX
Affiliate Professor - Department of Biological Sciences, Florida Atlantic University, Boca Raton, FL
Affiliate Professor - Florida Atlantic College of Medicine, Boca Raton, FL
Ph.D., University of California, Davis, 1979
Postdoctoral, California Institute of Technology, 1983
Department of Neuroscience
130 Scripps Way C349
Jupiter, Florida 33458
We pursue several different lines of research that fall within our interest in memory formation and the disorders of memory. We approach the complexities of the brain using multiple levels of analysis. At the molecular level, our goals are to understand the structure, regulation, evolution and biological function of genes required for normal memory formation. At the cellular level, the goal is to understand how the gene products mediate physiological changes after learning in the neurons that mediate behavior. An additional goal is to understand how alterations in neuronal physiology produce changes in communication with neighboring neurons that comprise the behavioral circuits. We also translate our basic science discoveries towards dissecting memory disorders in humans.
One current line of research continues our long-standing interest in the biology of memory formation using the fly, Drosophila. We have studied numerous genes in the past that are required for memory formation. Flies defective in the expression of these genes exhibit poor memory formation after olfactory conditioning tasks. We are continuing to study genes and gene products that influence memory formation but have recently moved the focus towards memory suppressor genes, genes whose disruption increases memory formation. This class of genes, which includes both protein coding genes and microRNA genes, are particularly interesting since they define the molecular constraints on memory formation – one way in which the brain manages memory systems – whether the genes participate by constraining acquisition or memory consolidation, or participate through involvement in active forgetting processes. A good example of an acquisition suppressor is DmSLC22A, a plasma membrane transporter that functions to remove cholinergic compounds from the synaptic cleft.
We have developed a powerful new imaging technology that allows us to visualize changes that occur in the brain of Drosophila due to learning. Using this technology, we have discovered several of these changes, or memory traces, in different neurons of the brain. Some changes occur immediately after learning and persist for only a few minutes; others form with a delay of up to several hours and likely persist for days. Thus, behavioral memory may be due to the effects of multiple memory traces, each controlling behavior over discrete windows of time after learning. We also use functional imaging technology to also visualize the process of active forgetting; watching the activity of dopaminergic neurons that mediate forgetting in head-fixed flies under the microscope as they exhibit locomotor activity or inactivity, including sleep, on a floating ball.
A second line of research has focused on the genetics and pathophysiology of bipolar disorder. This disorder affects about 2% of the population and involves rapid and extreme swings in mood state, from mania to severe depression. We identified a region of the genome the resides on the PDE10A gene that influences susceptibility to bipolar disorder, and have conducted deep, postmortem RNA sequencing experiments to detect differences in gene expression between the healthy and bipolar brain.
A third line of research focuses on the function of mitochondria in both healthy and disease states. Mitochondria are the energy powerhouses for all cells and become defective in the vast majority of neurological and psychiatric disorders. We have established new cell based screening techniques to identify small molecules that influence mitochondrial dynamics and function. This research is continuing with the goals of developing both probes and potential therapies associated with mitochondrial dysfunction.
Tomchik, S.M. and Davis, R.L. (2008). Cyclic AMP imaging sheds light on PDF signaling in circadian clock neurons. Neuron 58, 161-163.
Liu, X. and Davis, R.L. (2009). The GABAergic anterior paired lateral neuron of Drosophila suppresses and is suppressed by olfactory learning. Nat. Neurosci. 12, 53-59.
Tomchik, S. and Davis, R.L. (2009). Dynamics of learning-related cAMP signaling and stimulus integration in the Drosophila olfactory pathway. Neuron 64, 510-521.
Davis, R.L. (2011). Traces of Drosophila Memory. Neuron 70, 8-19.
Berry J.A., Cervantes-Sandoval, I., Nicholas, E.P., Davis, R.L. (2012). Dopamine is required for learning and forgetting in Drosophila. Neuron74, 530-542.
Berry, J.A., Cervantes-Sandoval, I., Chakraborty, M., Davis, R.L. (2015). Sleep facilitates memory by blocking dopamine neuron mediated forgetting. Cell 161, 1656-1667.
Guven-Ozkan, T., Busto, G.U., Schutte, S.S., Cervantes-Sandoval, I., O’Dowd, D. and Davis, R.L. (2016). MiR-980 is a memory suppressor microRNA that regulates the autism-susceptibility gene, A2bp1. Cell Reports 14, 1-12.
Gai, Y., Liu, Z., Cervantes-Sandoval, I. and Davis, R.L. (2016). Drosophila SLC22A transporter is a memory suppressor gene that influences cholinergic neurotransmission to the mushroom bodies. Neuron 90, 1-15.
Awards, Recognition, Appointments, and Honors
McKnight Scholars Award in Neuroscience from the McKnight Foundation
Development Award in Neuroscience from the McKnight Foundation
NIH Academic Career Leadership Award
McKnight Neuroscience of Brain Disorders Awardee
NARSAD Distinguished Investigator Award
Ellison Medical Foundation Senior Scholar in Aging Award
Jacob Javitts Career Award from the National Institutes of Health