B.S., Bloomfield College, 1974 Ph.D., University of California at San Diego, 1978 Faculty Fellow, National Institutes of Health Faculty Fellow, National Institute for Neurological and Communicative Disorders and Stroke
Dr. Farley studies the cellular and molecular bases of behavioral and neural plasticity, particularly those which involve changes in the biophysical properties of excitable membranes. Using voltage- and patch-clamp recording techniques with native neuronal membranes and artificial bilayers, as well as site-directed mutagenesis studies of cloned ion channel subunits in heterologous expression systems (e.g., Xenopus oocytes), he studies the cellular and molecular bases of associative learning in invertebrates and cellular models of memory (e.g., LTP) in the mammalian brain. Changes in potassium and calcium ion channels, their contributions to cellular mechanisms of coincidence- and non-coincidence detection, and the molecular mechanisms underlying those changes, such as protein kinase C-, PKA, tyrosine kinase-, and phosphatase-dependent (PP1, PP2B) changes in channel activities are of current interest.
Farley, J. and Han, Y. (1997). Learning-correlated changes in a delayed K+ current in Hermissenda Type A photoreceptors. Journal of Neurophysiology, 77, 1861-1888.
Britton, G. and Farley, J. (1999). Behavioral and neural bases of noncoincidence learning in Hermissenda. Journal of Neuroscience, 19(20), 9126-9132.
Farley, J. (2001). Modulation of rat brain synaptosomal calcium-activated potassium channels by protein kinases A and C, in press.
Huang, H. & Farley, J. (2001). PP1 inhibitors depolarize Hermissenda photoreceptors and reduce K currents. Journal of Neurophysiology, in press.
Jin, I. & Farley, J. (2001). Protein tyrosine kinase involvement in learning-produced changes in Hermissenda Type B photoreceptors. Journal of Neurophysiology, in press.
Last updated:
June 6, 2001
URL: http://www.indiana.edu/~neurosci/farley.html
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Indiana University