olds@helix.nih.gov (James Olds) (05/01/91)
I am interested in the role of protein kinase C in neuronal plasticity. Initially we were able to report changes in the distribution of this critical enzyme within the hippocampus during classical conditioning and other forms of learning in rabbit, rat and the marine snail, Hermissenda. More recently, myself and Dr. JV Sanchez-Andres have been pursuing studies on the distributional changes in PKC as assessed by quantitative autoradiography, within the neonatal rabbit hippocampus. In addition to the quantitative autoradiography studies, we have also been studying the electrophysiology of neonatal CA1 pyramidal cells. What follows is information that we are abstracting to the Society for Neuroscience for the November 1991 meetings: CA1 cells recorded from littermates showed a characteristic pattern, consisting of A) adaptation, associated with B) firing a small number of spikes (1-3) when a depolarizing pulse was applied. By Day 15 post partum, all cells showed the adult pattern consisting of a moderate adaptation which slowed down the spiking frequency along a depolarizing pulse. The change of pattern was associated temporally with the day in which the Neonates opened the eyes (NEO). The pattern of PKC distribution seen before NEO was qualitatively different from that seen either after that point in developement or in adults. This was manifested by extremely dense bands of 3H-phorbol ester binding on either side of the stratum pyramidale both in CA1 and in CA3. These bands dramatically delineated the cell body layer and were localized to the most proximate apical and basilar dendritic zones. After NEO, this pattern shifted to one reminiscent of that seen in an adult classically conditioned animal 24 h into retention (i.e stratum oriens and pyramidale showing together the greatest binding; Olds et al. Science 1989). We are interested in what other members of the neuroscience community make of these results. We are especially interested in possible interpretations of the activated PKC as zones of *inactivated* potassium channels. Finally we would be very interested in the theoretical implications of such phenomena in the hippocampus during this critical developmental period. -- ************************************************************************ ***** * James L. Olds Ph.D. Laboratory of Cellular and Molecular Neurobiology* * domain:olds@helix.nih.gov NINDS, NIH, Bethesda, MD. 20892 USA * ************************************************************************ *****