The sophisticated cognitive functions of the human brain reside in complex connections of cells in the central nervous system. Communication between nerve cells, via synaptic transmission, is a highly plastic process, with signal strength waxing and waning as new information is processed and stored. One of the major challenges of modern neuroscience is to understand synaptic plasticity, with the hope that this will lead to deeper insights about our own ability to learn and remember.
Research in my laboratory has been directed toward understanding mechanisms that initiate and regulate changes in synaptic strength. Our recent work, described in more detail below, has focused on elucidating fundamental biophysical characteristics of membrane proteins that control an early event in the process: the influx of extracellular calcium into the interior of nerve cells. Rapid calcium entry in nerve cells is accomplished by proteins known as calcium channels, which can be opened to allow calcium passage. Calcium channels can be activated by electrical signals (changes in intracellular voltage) or by chemical ones (such as the neurotransmitter glutamate). By working with isolated neurons in tissue culture, we have recently identified a new type of voltage-gated calcium channel and a novel effect of the brain-derived neurotrophic factor (BDNF) on the NMDA receptor. Future studies will involve expanding the functional context in which these proteins are examined, moving from isolated cells to the sophisticated neuronal assemblies found in brain slices. The ultimate goal that guides us will be to answer the question of how the properties and modulation of calcium-permeable membrane proteins lead to stimulus-specific control of synaptic strength.