Director; Ctr for Learning and Memory, Institute for Neuroscience
Chairman, Section of Neurobiology
Karl Folkers Chair in Interdisciplinary Biomedical Research
Main Office: NHB 2.504
Alternate Office: NHB 2.310
Alt. Phone: 512-475-7905
The University of Texas at Austin
Ctr for Learning and Memory
1 University Station
Austin ,TX 78712
Research in my laboratory is primarily directed towards understanding the cellular and molecular mechanisms of synaptic integration and long-term plasticity of neurons in the medial temporal lobe. We have focused our attention on the hippocampus, subiculum, and entorhinal cortex, areas of the brain that play important roles in learning and memory. These regions are also of interest because they have a low seizure threshold and are implicated in several forms of human epilepsy. Our research uses quantitative electrophysiological, optical-imaging, and computer-modeling techniques.
We are investigating long-term synaptic potentiation and depression, forms of plasticity thought to underlie aspects of memory. This interest has led us to investigate the basic mechanisms of synaptic integration in the dendrites of the neurons in these regions. We have used fluorescence imaging techniques and dendritic patch-clamp recordings to identify the types of voltage-gated ion channels (Na+, K+, Ca+, and h channels) expressed in dendrites of hippocampal and entorhinal cortex pyramidal neurons. We have also begun to identify changes in the properties and expression levels of some of these channels accompanying synaptic potentiation and depression. These studies have suggested that plasticity of intrinsic excitability of neurons is an important component of learning and memory. Our computer modeling studies, which reconstruct the biophysical properties of these neurons based on our experimental data, complement this work. We hope that these investigations will enhance our understanding of the neuronal mechanisms of learning and memory and provide insight into the function of the hippocampus and neighboring cortex in the normal behaving animal as well as under disease states such as epilepsy.