David Friel, PhD

Associate Professor
Department of Neurosciences
School of Medicine

Research Information

Research Interests

I am interested in how cells communicate and process information through the use of systems of interacting signaling molecules, especially ion channels, and transporters. Behind this interest is a desire to understand how the signaling mechanisms expressed in cells extract information from their environment to facilitate higher order function of cell assemblies.

Specific research projects in which this general question has been explored include:

  1. Cellular Ca2+ signaling in neurons, specifically addressing how Ca2+ channels and transporters at the cell surface and within the membranes of internal stores interact functionally to orchestrate Ca2+ signals in response to stimulation
  2. The impact of ataxia-producing mutations in the gene encoding P/Q type Ca2+ channels on membrane excitability, synaptic transmission and circuit properties in the cerebellar cortex.

I hope my research will provide insight into basic mechanisms of intra- and intercellular-communication, and point to new and effective approaches for overcoming Ca2+ regulatory disorders in humans.



View All Publications

Selected Publications

  1. Ovsepian SV, Friel DD. (2010)
    Enhanced Synaptic Inhibition Disrupts the Efferent Code of Cerebellar Purkinje Neurons in Leaner Ca(v)2.1 Ca (2+) Channel Mutant Mice. Cerebellum. 2010 Sept 16.
  2. Liu S, Friel DD. (2008)
    Impact of the leaner P/Q-type Ca2+ channel mutation on excitatory synaptic transmission in cerebellar Purkinje cells. J Physiol. 2008 Aug 14; 129(1):93-103.
  3. Ovsepian SV, Friel DD. (2008)
    The leaner P/Q-type calcium channel mutation renders cerebellar Purkinje neurons hyper-excitable and eliminates Ca2+-Na+ spike bursts. Eur J Neurosci. 2007 Dec 17; 27(1):93-103.
  4. Friel DD, Chiel HJ. (2008)
    Calcium dynamics: analyzing the Ca2+ regulatory network in intact cells. Trends Neurosci. 2007 Dec 4; 31(1):8-19.
  5. Patterson M, Sneyd J, Friel DD. (2007)
    Depolarization-induced calcium responses in sympathetic neurons: relative contributions from Ca2+ entry, extrusion, ER/mitochondrial Ca2+ uptake and release, and Ca2+ buffering. J Gen Physiol. 2007 Jan 1; 129(1):29-56.
  6. Jones SW, Friel DD. (2006)
    The amplitude distribution of release events through a fusion pore. Biophys J. 2006 Mar 1; 90(5):L39-L41.
  7. Albrecht MA, Colegrove SL, Friel DD. (2002)
    Differential regulation of ER Ca2+ uptake and release rates accounts for multiple modes of Ca2+-induced Ca2+ release. J Gen Physiol. 2002 Mar; 119(3):211-233.
  8. Albrecht MA, Colegrove SL, Hongpaisan J, Pivovarova NB, Andrews SB, Friel DD. (2001)
    Multiple modes of calcium-induced calcium release in sympathetic neurons I: attenuation of endoplasmic reticulum Ca2+ accumulation at low [Ca2+]i during weak depolarization. J Gen Physiol. 2001 Jul; 118(1):83-100.
  9. Hongpaisan J, Pivovarova NB, Colegrove SL, Leapman RD, Friel DD, Andrews SB. (2001)
    Multiple modes of calcium-induced calcium release in sympathetic neurons II: a [Ca2+](i)- and location-dependent transition from endoplasmic reticulum Ca accumulation to net Ca release. J Gen Physiol. 2001 Jul; 118(1):101-112.
  10. Colegrove SL, Albrecht MA, Friel DD. (2000)
    Quantitative analysis of mitochondrial Ca2+ uptake and release pathways in sympathetic neurons. Reconstruction of the recovery after depolarization-evoked [Ca2+]i elevations. J Gen Physiol. 2000 Mar; 115(3):371-388.
  11. Colegrove SL, Albrecht MA, Friel DD. (2000)
    Dissection of mitochondrial Ca2+ uptake and release fluxes in situ after depolarization-evoked [Ca2+](i) elevations in sympathetic neurons. J Gen Physiol. 2000 Mar; 115(3):351-370.
  12. Pivovarova NB, Hongpaisan J, Andrews SB, Friel DD. (1999)
    Depolarization-induced mitochondrial Ca accumulation in sympathetic neurons: spatial and temporal characteristics. J Neurosci. 1999 Aug 1; 19(15):6372-84.
  13. Friel DD. (1995)
    [Ca2+]i oscillations in sympathetic neurons: an experimental test of a theoretical model. Biophys J. 1995 May; 68(5):1752-1766.



Doctor of Philosophy
University of Chicago