PhD, University of Virginia
Neuronal Mechanisms of Memory and Aging
After serving as an avionics electronics technician maintaining fighter aircraft in the US Air Force, Dr. Lucien T. "Tres" Thompson received his undergraduate degree in Psychology & Biology and masters degree in Experimental Psychology from California State University, San Bernardino. While there, he received training in wildlife biology, animal behavior, and human electrophysiology, and carried out diverse experimental studies using taste aversion to alter predatory behaviors of wild coyotes and using biofeedback to enhance the human relaxation response (EEG alpha rhythm).
Crossing the continent, Dr. Thompson became a Thomas Jefferson Presidential Scholar at the University of Virginia, Charlottesville, Virginia, earning his PhD in Neuroscience for his work on the stability and plasticity of hippocampal place cells. Additional post-doctoral training in neurophysiology and neurobiology occurred at Northwestern University Medical School in Chicago, where Dr. Thompson wrote a number of well-funded RO1s which allowed him to remain as a research faculty member in the Department of Cell, Molecular & Structural Biology, studying cellular mechanisms of associative learning in aging humans and in model systems. His research interests in substances that can enhance memory (nootropics) developed at Northwestern.
At the inauguration of a new Neuroscience program at UT Dallas in 1997, Dr. Thompson became half of the starting faculty, and has overseen the program's rapid and successful growth. Besides PhDs mentored in Chicago, seven new PhDs have emerged from his Aging & Memory laboratory here in BBS, with several now themselves faculty in the neurosciences at other universities.
As a cellular- and systems-level neuroscientist, I strive to understand and improve the basic cellular mechanisms of learning and memory. I have concentrated my research efforts on regulation of post-synaptic excitability, more specifically, the necessary role of Ca2+-dependent K+ channels.
These K+ channels play a crucial role in memory-related plasticity across the lifespan. They interact strongly with NMDA (NR) excitatory glutamate receptors to regulate excitability in Hebbian models, and bridge important gaps in multiple forms of meta-plasticity critical for memory consolidation. Our work shows that plasticity of these K+ channels is highly conserved: across different species, different tasks, and across brain regions (i.e. they are a necessary convergence point in learning and in memory consolidation).
Our learning and memory research incorporates both chronic in vivo and acute in vitro neurophysiological recordings, coupled with molecular/neurochemical assays, as well as a wide range of behavioral approaches. Recent investigations have assessed the effects of channel-specific antagonists, of anti-oxidants, stress, and emotion, and have manipulated or assessed cellular mechanisms in experience- and aging-dependent neuropathologies including tinnitus and diabetes. Our data clearly demonstrate adaptive shifts in cognitive and neurobiological strategies for storing and accessing memories as the brain ages, yielding new potential nootropic targets for functional improvement (i.e. better memory).
Farmer, G.E. & Thompson, L.T. (2012). Learning-dependent plasticity of hippocampal CA1 pyramidal neuron post-burst afterhyperpolarizations and increased excitability after inhibitory avoidance learning depend upon basolateral amygdala inputs. Hippocampus, 22, 1703-1719.
Goble, T.J., Møller, A. & Thompson, L.T. (2009). Acute high-intensity sound exposure alters responses of place cells in hippocampus. Hearing Research, 253, 52-59.
Greer, T.L., Trivedi, M.H. & Thompson, L.T. (2005). Impaired delay and trace eyeblink conditioning performance in major depressive disorder. Journal of Affective Disorders, 86, 235-245.