UTSA Biology Faculty
David B. Jaffe, Ph.D.
Associate Professor of Neurobiology
Office: SCB 3.01.25
Phone: (210) 458-5843
David.Jaffe@utsa.edu
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Research Interests
Research in my laboratory focuses on the hippocampal formation; a brain region important for certain aspects of learning and memory. It is also one of the first brain structures affected by Alzheimer's disease and and medial temporal lobe epilepsy arises in the hippocampus, among other brain structures.
Our major area of interest is the CA3 region of the hippocampus. This subregion is where information from two regions outside the hippocampus, the dentate gyrus and the entorhinal cortex, converge. In addition, this area is also characterized by strong recurrent feedback between CA3 pyramidal neurons forming what is thought to be an autoassociative network. Artificial neural networks composed of such circuits perform pattern completion. Under pathalogical conditions, this circuity is what makes area CA3 highly susceptible to epilepsy.
Current work in the laboratory focuses on two questions. First, what are the input/output characteristics of CA3 pyramidal neurons? We are interested in how the morphology and distribution of ion channels in these cells interact to process, encode, and retrieve synaptically-based information. Understanding how these cells integrate synaptic information is important for understanding the functional role of this network during normal circumstances and under pathophysiological conditions, for example in the case of epilepsy. Our second question concerns how the properties of neurons and synapses within area CA3 change in aged animals. It is well known that aged animals are cognitively impaired and this correlates with a number of cellular changes that occur with senescence. The laboratory is testing whether some of these changes might actually be compensatory. That is, in response to pathophysiological changes that occur with age, such as the loss of receptors associated with synaptic, certain changes in excitability or synaptic inhibition may enhance functional aspects of the network as it ages.
Recent Publications
Hemond, P. and Jaffe, D.B., Caloric restriction prevents aging-associated changes in spike-mediated Ca2+ accumulation and the slow afterhyperpolarization in hippocampal CA1 pyramidal neurons, Neurosci., 135:413-420, 2005.
Gamper, N, Zaika, O, Li, Y., Martin, P, Hernandez, C, Perez, M, Wang, A.Y.C, Jaffe, D.B., and Shapiro, M.S. Oxidative Modification of M-type Potassium Channels as the Mechanism of Cytoprotective Neuronal Silencing, EMBO Journal, 25:4996-5004, 2006.
Zaika, O, Lara, L, Gamper, N, Hilgemann, Jaffe, D, and Shapiro, M., Mechanism and functional role of angiotensin ii regulation of Kv7 (M-type) K+ channels, J. Physiol., 575:46-67, 2006.
