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Colin Heath

Colin Heath,  BSc, PharmD
Postdoctoral Fellow,
University of Calgary, In Progress
Hotchkiss Brain Institute
Health Research Innovation Center (HRIC) 1B42A
University of Calgary
Calgary Alberta Canada
T2N 4N1
Phone: 403-220-8451
FAX: 403-210-7446
ncheath@ucalgary.ca

Training
PharmD 2010
Massachusetts College of Pharmacy and Health Sciences
Boston, Massachusetts

BSc Psychology 2012
Department of Psychology
University of Calgary
Calgary Alberta

Awards
PharmD
CVS academic achievement award
Canadian Achievement Award
Rho Chi Honors Society member


Research Focus: The Cav3-Kv4 signaling complex in cerebellar signal processing
Approach: I use patch clamp recordings in vitro to determine the ability for cerebellar cells to incorporate the activity of a novel Cav3-Kv4 complex in signal processing
Preparations: In vitro slice preparation, modeling, dynamic clamp
Below are short summaries of my projects published from the lab.
Biocytin-filled DCN neuron and MAP-2 labeled dendritic processes

Model - Cerebellar granule cells
    Granule cells make up the input layer of cerebellum, receiving mossy fiber synaptic input that conveys sensory information, and project parallel fiber axons to the cerebellar cortex. Granule cells have long been known to express the A-type, Kv4 class of fast inactivating potassium channel. I study the role of Kv4 channels in controlling the excitability and spike output of granule cells using patch clamp recordings in an in vitro slice preparation.

A Cav3-Kv4 complex acts as a novel calcium sensor in stellate cells A novel calcium sensor dynamically adjusts inhibitory charge transfer to Purkinje cells
   Stellate cells were known to inhibit complex spikes of Purkinje cells but a mechanism that would allow them to respond to local repetitive climbing fiber input was unknown. This study shows that a Cav3-Kv4 complex expressed in stellate cells acts as a novel calcium sensor to dynamically adjust stellate cell frequency in relation to changes in [Ca]o during complex spike discharge. Inhibitory charge transfer to Purkinje cells is thus maintained in the face of a synaptically evoked decrease in [Ca]o that would otherwise alter network function. See Anderson et al. (2013).
A Cav3-Kv4 complex differentially modifies cerebellar granule cell excitability The expession pattern of subunits for the Cav3-Kv4 complex regulates granule cell output
   A compartmentalization of function in cerebellum begins with a segregation of mossy fibers across ten distinct lobules, with tactile receptor inputs in anterior lobules and vestibular input in caudal lobules. A dense expression of T-type calcium channels in lobule 9 granule cells selectively augments Kv4 current to lower the gain of firing compared to lobule 2 cells. The Cav3-Kv4 complex then proves to enable a more stable tonic firing capability in lobule 9 cells well suited to processing vestibular-like input compared to burst input in lobule 2 cells. Heath et al. (2014).
IKCa channels are a major determinant of the CA1 hippocampal pyramidal cell sAHP IKCa channels are a critical determinant of the CA1 pyramidal cell slow AHP
   CA1 pyramidal cells have been shown to express immunolabel and promoter activity of the IKCa channel. Recordings of the slow AHP in CA1 pyramidal cells revealed single channels that match the pharmacological profile of IKCa channels, which prove to underlie the long duration slow AHP. Block of IKCa channels confirm a key role in reducing temporal summation of EPSPs and mediating spike accommodation. (see King et al. (2015)).

Peer Reviewed Publications

Anderson, D.*, Engbers, J.D.T.*, Heath, N.C., Bartoletti, T.M., Mehaffey, W.H., Zamponi, G.W., and Turner, R.W. (2013) The Cav3-Kv4 complex acts as a calcium sensor to maintain inhibitory charge transfer during extracellular calcium fluctuations. J. Neuroscience 33: 7811-7824. * Shared first authors.
PDF

Heath, N.C., Rizwan, A.P., Engbers, J.D.T., Anderson, D., Zamponi, G.W. and Turner, R.W. (2014) The expression pattern of a Cav3-Kv4 complex differentially regulates spike output in cerebellar granule cells. J. Neuroscience 34(26): 8800-8812.

King, B.*, Rizwan, A.P.*, Asmara, H., Heath, N.C., Engbers, J.D.T, Dykstra, J., Bartoletti, T.M., Hameed, S., Zamponi, G.W., and Turner, R.W. (2015) IKCa channels are a critical determinant of the slow AHP in CA1 pyramidal neurons. Cell Reports. 11:1-8. *Shared first authors. Link

Abstracts - Published work.

Heath, N.C., Pervaiz, A., Anderson, D., Engbers, J.D.T. and Turner, R.W.  Postsynaptic excitability of granule cells is differentially regulated across cerebellar lobules by a Cav3-Kv4 channel complex. Can. Assoc. Neurosci., 2013.

Anderson, D.*, Engbers*, J.D.T., Heath, N.C., Bartoletti, T.M., Mehaffey, W.H., Zamponi, G.W. and Turner, R.W. The Cav3-Kv4 complex acts as a calcium sensor to adaptively modulate inhibitory network function during repetitive excitatory input. Can. Assoc. Neurosci., 2013.

Heath, N.C., Pervaiz, A., Anderson, D., Engbers, J.D.T. and Turner, R.W. Postsynaptic excitability of granule cells is differentially regulated across cerebellar lobules by a Cav3-Kv4 channel complex. Cerebellar Gordon Conference, 2013.

Heath, N.C.*, Pervaiz, A.*, Anderson, D., Engbers, J.D.T. and Turner, R.W.  Postsynaptic excitability of granule cells is differentially regulated across cerebellar lobules by a Cav3-Kv4 channel complex. Can. Assoc. Neurosci., 2013

Anderson, D.*, Engbers*, J.D.T., Heath, N.C., Bartoletti, T.M., Mehaffey, W.H., Zamponi, G.W. and Turner, R.W.  The Cav3-Kv4 complex acts as a calcium sensor to adaptively modulate inhibitory network function during repetitive excitatory input. Can. Assoc. Neurosci., 2013

Heath, N.C., Pervaiz, A., Anderson, D., Engbers, J.D.T. and Turner, R.W.  Postsynaptic excitability of granule cells is differentially regulated across cerebellar lobules by a Cav3-Kv4 channel complex. Gordon Conference, Cerebellum 2013.

Asmara, H., Heath N.C., Simms, B., Bartoletti, T.M., Rehak, R., Micu, I., Zhang, F.X., Stys, P., Zamponi, G.W. and Turner, R.W. T-type calcium channels form a calcium-dependent complex with calmodulin. Proc. Soc. Neurosci., 2014.

King, B., Rizwan, A. P., Heath, N.C., Asmara, H., Dykstra, S., Zamponi, G.W. and Turner, R.W. Novel roles for IKCa channels in rodent hippocampal CA1 pyramidal neurons. Proc. Soc. Neurosci., 2014.

King, B.*, Rizwan, A.P.*, Heath, N.C., Asmara, H., Dykstra, S., Zamponi, G.W. and Turner, R.W.  IKCa channels are a critical determinant of the slow AHP in hippocampus.  Can. Assoc. Neurosci., 2015.

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