David L. Glanzman
| dglanzman@physci.ucla.edu | |
| Office phone | (310) 206-9972 |
| Lab phone | (310) 206-4852 |
| address | 695 Young Drive South, Box 951761, Los Angeles, CA 90095-1761 |
| office | 2506 C Gonda Center |
| Lab | 2524 Gonda Center |
research interests: Neurobiology
of Learning and Memory
education:
B. A., Indiana University, 1973
Ph.D. Stanford University, 1980
Postdoctoral Fellow, UCLA, 1980-1983
Research Associate, Howard Hughes Medical Institute, Columbia University, 1984-1990
My laboratory's interests are in the cell biology of learning and memory in the marine snail Aplysia californica. This animal has a relatively simple nervous system that provides a valuable experimental model for analysis of the cellular mechanisms underlying simple forms of learning, such as habituation, sensitization, and classical conditioning. Another experimental advantage of Aplysia is that the sensory and motor neurons which mediate specific reflexes may be dissociated from the animal’s nervous system and placed into cell culture, where they will reform their original synaptic connections. These in vitro sensorimotor synapses are ideal for cellular studies of synaptic plasticity, involving such techniques as intracellular electrophysiology, whole-cell recording with patch pipettes, and imaging of activity-associated changes in intracellular calcium and using fluorescent dyes.
We have found that Aplysia sensorimotor synapses in cell culture exhibit both long-term potentiation (LTP) and long-term depression (LTD), two forms of synaptic plasticity thought to play critical roles in associative learning in vertebrates. We now have evidence that LTP mediates classical conditioning of the withdrawal reflexes of Aplysia. In future research we will explore the potential interaction between LTP and serotonin, a modulatory transmitter in the nervous system of Aplysia; determine the cellular processes that underlie the induction and expression of LTP of in vitro Aplysia synapses; and attempt to define the role of LTD in Aplysia learning.
Publications
Murphy, G.G., and Glanzman, D.L. (1999) Cellular analog of differential classical conditioning in Aplysia: disruption by the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate. Journal of Neuroscience 19: 10595-10602.
Murphy, G.G., and Glanzman, D.L. (1997) Mediation of classical conditioning in Aplysia californica by LTP of sensorimotor synapses. Science 278: 467–471.
Murphy, G.G., and Glanzman, D.L. (1996) Enhancement of sensorimotor connections by conditioning-related stimulation in Aplysia depends upon postsynaptic Ca2+. Proceedings of the National Academy of Sciences USA 93: 9931–9936.
Lin, X.Y., and Glanzman, D.L. (1994) Hebbian induction of long-term potentiation of Aplysia sensorimotor synapses: partial requirement for activation of an NMDA-related receptor. Proc. R. Soc. Lond. B 255: 215-221.
Murphy, G.G., and Glanzman, D.L. (1996) Enhancement of sensorimotor connections by conditioning-related stimulation in Aplysia depends upon postsynaptic Ca2+. Proceedings of the National Academy of Sciences USA 93: 9931–9936.
Murphy, G.G., and Glanzman, D.L. (1997) Mediation of classical conditioning in Aplysia californica by LTP of sensorimotor synapses. Science 278: 467–471.