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Dustin Anderson  PhD/MD Student
DiplT Electronics Engineering Technology BCIT
BSc Simon Fraser University

PGY1, Neurology
University of Alberta
Department of Medicine
13-103 Clinical Sciences Building
11350 - 83 Avenue
Edmonton, Alberta, Canada
T6G 2G3
dustin3@ualberta.ca

Training
2002
DiplT Electronics Engineering Technol.
BC Institute of Technology
Vancouver Canada

2007
BSc Cell Molecular Biology
Simon Fraser University
Vancouver Canada

2007 - 2014
PhD / MD
University of Calgary
Supervisors: R.W. Turner/G.W. Zamponi

Special Courses
2008
Frontiers in Neurophotonics
Laval University
     
Awards
BSc
2005
- SFU Open Scholarship
Golden Key Int. Honours Soc.



2006
- John and Isabel Young Bursary
- SFU Open Scholarship
- SFU Alumni Scholarship


2007
- SFU Open Scholarship
- SFU Alumni Scholarship
- Nat. Neurosci. Compet., UofC

PhD
- Achievers in Medical Science (AIMS)
- Chen Fong Scholarship HBI
- Queen Elizabeth II Scholarship

- TA Cellular & Molecular Neuroscience
- AIMS Excellence in Research (2)
- MDNS Program Specific Award (3)
- Dean's Publication and Mentorship Prize 2010
- Dean's Publication and Mentorship Prize 2011
- Leaders in Medicine Program
- AHFMR Studentship
- I. Walton Killam Scholarship
- Silver Medal, CIHR National Research Poster Competition
- Governor General 's Gold Medal Award - PhD 2011
- Dept. Neuroscience nominee - CAGS/UMI Distinguished Dissertation Award 2012
- Leaders in Medicine - AIMS Excellence in Research award
 
Research Focus: The basis of T type ion channel interactions
Approach: Electrophysiology in vitro, pharmacology, two-photon imaging
Preparations: In vitro slice preparations, tissue sections
Below are short summaries of projects published from my research.
Biocytin-filled DCN neuron and MAP-2 labeled dendritic processes Model - Stellate cells
    Cerebellar stellate cells respond to membrane hyperpolarizations with a non-monotonic first spike latency due to the co-expression of T-type calcium and A-type potassium channels. My project focuses on the interplay between these currents that determine the timing of first spike discharge following membrane hyperpolarizations.

Representative examples of Transient and Weak Burst Cell spike rebounds Distinct ion channel contributions to burst phenotype in deep cerebellar neurons
    The large diameter putative projection neurons of rat deep cerebellar nuclei have been shown to generate either a Transient or Weak rebound Burst phenotype that was linked to the selective expression of T-type calcium channel isoforms. Here we show that the two burst phenotypes also reflect a differential functional availability of LVA T type calcium current at burst threshold, and different contributions of repolarizing potassium currents that shape burst properties. See Molineux et al. (2008). PDF
On-cell and Whole-cell recording of DCN cell rebound Synaptically evoked rebound bursts in deep cerebellar neurons
    Rebound burst discharge in deep cerebellar nuclear (DCN) cells is readily evoked through direct current injection, but the probability of evoking rebounds with inhibitory synaptic stimulation is less certain. Here we show that stimulation of Purkinje cell inhibitory inputs to DCN neurons in vitro evokes rebound bursts that can be distinguished according to two known phenotypes of burst output. Reliable rebound burst generation indicates the potential for this activity to contribute to cerebellar output in response to physiological activity in vivo. See Tadayonnejad et al. (2009). PDF
KChiP3 mediated shift in Kv4 inactivation A Cav3-Kv4 signaling complex regulates A type current and neuronal activity
   A-type potassium channels of the Kv4 family regulate the latency and frequency of spike output in numerous CNS cells. Kv4 channels complex with Potassium Channel Interacting Proteins (KChIPs), a family of calcium sensor proteins that should confer calcium sensitivity. However, neither the physiological source for calcium nor its effects on A-type current were known. Here we show that T-type (Cav3) calcium channels associate with the Kv4 complex to selectively modulate Kv4 inactivation and establish function in a physiological range. See Anderson et al. (2010). PDF
Cav3.1 channels link to Kv4.2 channels The Cav3.1 calcium channel modulates Kv4.2 voltage for inactivation
   Here we show that the Cav3.1 (T-type) calcium channel isoform also associates with the Kv4.2 complex to selectively right-shift Kv4 inactivation, but to a lesser extent than for other Cav3 channel isoforms. A link between Cav3.1 and Kv4.2 is further indicated through coimmunoprecipitation and pulldowns with Cav3.1 fusion proteins.
See Anderson et al. (2010b). PDF
IT and IH have distinct roles in DCN rebound bursts Distinct roles for IT and IH in controlling deep cerebellar rebound responses
   Here we examined the role for IT and IH in generating the rebound responses that are evoked in deep cerebellar neurons in response to inhibitory input from Purkinje cells. We used recordings in vitro and modeling to find that only a small fraction of the total IT and IH available to a cell are activated by physiological levels of hyperpolarization. However, the currents activated are still sufficient to differentially control the latency, frequency and precision of spike firing during the immediate phase of a rebound response. See Engbers et al. (2011). PDF
Charybdotoxin slows the rate or repolarization of the parallel fiber-evoked EPSP An intermediate conductance KCa channel modifies parallel fiber EPSPs in Purkinje cells
   Purkinje cells were known to express the two KCa channels typically found in central neurons (SK and BK channels). This study reports that the intermediate conductance KCa channel (KCa3.1) is also expressed in Purkinje cells and is linked to Cav3.2 T-type calcium channels. KCa3.1 is activated during the parallel fiber EPSP to increase the EPSP rate of decay and generate a long duration AHP to suppress temporal summation of low frequency EPSPs, allowing Purkinje cells to respond to sensory-like bursts of parallel fiber input. Engbers et al. (2012). PDF
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). PDF
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).

Peer-reviewed Publications

Molineux, M.L., Mehaffey, W.H., Tadayonnejad, R., Anderson, D., Tennent, A.F. and Turner, R.W. (2008) Ionic factors governing rebound burst phenotype in rat deep cerebellar neurons. J. Neurophysiology 100:2684-2701. PDF

Tadayonnejad, R., Mehaffey, W.H., Anderson, D. and Turner, R.W. (2009) Reliability of triggering postinhibitory rebound bursts in deep cerebellar neurons. Channels 3(3): 149-155. Open Access.

Anderson, D., Mehaffey, W.H., Iftinca, M., Rehak, R., Engbers, J.D.T., Hameed, S., Zamponi, G.W. and Turner, R.W.  (2010) Regulation of neuronal activity by Cav3-Kv4 channel signaling complexes.  Nature Neuroscience 13: 333-337. Link  Faculty of 1000 citation. PDF

Anderson, D., Rehak, R., Hameed, S., Mehaffey, W.H., Zamponi, G.W. and Turner, R.W. (2010) Regulation of the Kv4.2 complex by Cav3.1 channels. Channels 4(3): 163-167. Open Access PDF

Engbers, J.D.T.*, Anderson, D.*, Tadayonnejad, R.*, Mehaffey, W.H., Molineux, M.L. and Turner, R.W. (2011) Distinct roles for IT and IH in controlling the frequency and timing of rebound spike responses. J. Physiol (Lond.), 589 (Pt 22): 5391-413. * Shared first authors. PDF

Engbers, J.D.T.*, Anderson, D.*, Asmara, H., Rehak, R., Mehaffey, W.H., Hameed, S., McKay, B.E., Kruskic, M., Zamponi, G.W. and Turner, R.W. (2012) Intermediate conductance calcium-activated potassium channels modulate summation of parallel fiber input in cerebellar Purkinje cells. PNAS 109 (7): 2601-2606. * Shared first authors. Faculty of 1000 citation. PDF

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..


Invited Chapters / Reviews

Tadayonnejad, R., Anderson, D., Molineux, M.L., Mehaffey, W.H., Jayasuriya, K. and Turner, R.W. (2011) Rebound discharge in deep cerebellar nuclear neurons in vitro. Cerebellum 9(3): 352-374. PDF

Turner, R.W., Anderson, D. and Zamponi, G.W. (2011) Signaling complexes of voltage gated calcium channels. Channels 5(5): 440-448.

McKay, B.E., Tadayonnejad, R., Anderson, D., Engbers, J.D.T., Fernandez, F.R.,  Iftinca, M. and Turner, R.W. (2012)  Establishing in vivo like activity in rat cerebellar cells maintained in vitro. In Isolated Central Nervous System Circuits, (Ed K Ballanyi), Neuromethods Series Vol 73 (Ed W Walz). Springer Science+Business Media, LLC, New York, NY, pp 233-262. PDF

Engbers, J.D.T., Anderson, D., Zamponi, G.W. and Turner, R.W. (2013) Signal processing by T-type calcium channel interactions. Invited review,Frontiers in Cellular Neuroscience 7 (230): 1-15. PDF.


Invited Talks

Department of Neurobiology, Harvard Medical School, Boston MA. The Cav3-Kv4 complex.

Key Abstracts - Published work

Iftinca M, Anderson D., Rehak, R., Molineux, M.L., McRory, J., Zamponi, G.W. and Turner, R.W.   T-type calcium channels provide calcium-dependent modulation of A-type potassium channels. Can. Assoc. Neurosci. Montreal  2008.

Anderson, D., Mehaffey, W.H., Engbers, J.D.T, Rehak, R., Hamid, S., Zamponi, G.W. and Turner, R.W. T-type mediated calcium influx dynamically modulates Kv4 inactivation.  Can. Assoc. Neurosci. Vancouver  2009.

Anderson, D., Iftinca, M., Mehaffey, W.H., Rehak, R., Hami,d S., Zamponi, G.W. and Turner, R.W.  A-type potassium channels are dynamically regulated by T-type calcium current. IUPS  Kyoto 2009.

Turner, R.W., Anderson, D., Iftinca, M., Mehaffey, W.H., Rehak, R., Hamid, S., Zamponi, G.W. Regulation of neuronal activity by Cav3-Kv4 channel signaling complexes.  Ion Channels & Transporters Mtg, Lake Biwa, Kyoto Japan, 2009.

Anderson, D., Iftinca, M., Mehaffey, W.H., Rehak, R., Engbers, J.D.T., Hamid, S., Zamponi, G.W. and Turner, R.W.  Regulation of neuronal output by Cav3-Kv4 signalling complexes. Proc. Soc. Neurosci. 2009.

Tadayonnejad, R., Engbers, J.D.T., Anderson, D., Mehaffey, W.H. and Turner, R.W. The role of IH and IT in controlling rebound burst properties of Deep Cerebellar Nuclear cells. Can Assoc. Neurosci., 2010.

Tadayonnejad, R., Engbers, J.D.T., Anderson, D., Mehaffey, W.H. and Turner, R.W. IT and IH selectively regulate rate coding and spike precision in deep cerebellar nuclear cells. Proc. Soc. Neurosci., 2010.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Zamponi, G.W. and Turner, R.W.   T-type/IK channel signalling complex modulates summation of parallel fiber inputs in cerebellar Purkinje cells.  Can. Assoc. Neurosci. 2010.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Zamponi, G.W. and Turner, R.W.   IKCa channels establish a high pass filter for parallel fiber input in cerebellar Purkinje cells.  Gordon Conference, Cerebellum in Health and Disease, New London, NH, 2011.

Engbers, J.D.T., Anderson, D., Rehak, R., Asmara, H., Mehaffey, W.H., Hameed, S., McKay, B.E., Kruskic, M., Zamponi, G.W., Turner, R.W.  IKCa-Cav3 complex reduces temporal summation of parallel fiber input in cerebellar Purkinje cells. IBRO World Congress of Neuroscience, Florence, Italy, 2011.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Kruskic, M., Zamponi, G.W., Turner, R.W.  IKCa-Cav3 complex creates a high pass filter for parallel fiber input in cerebellar Purkinje cells. Comp. Neurosci., Stockholm, Sweden, 2011. Prize, Student Poster Presentation.

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.

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