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Jordan D.T. Engbers  PhD
University of Calgary, April 2013

Data Scientist / Postdoctoral Fellow
Clinical Research Unit

HMRB 193 University of Calgary
3330 Hospital Dr NW
Calgary Alberta Canada
T2N 4N1
Phone: 403-210-6372
jdtengbe@ucalgary.ca

Training
BHSc 2008, Bioinformatics
University of Calgary
Calgary Alberta

PhD 2013, Neuroscience
University of Calgary
Calgary Alberta

Special Courses
2008  -  Summer School in Computational Neuroscience
            University of Ottawa ON
         - Computational Cellular Electrophysiology
             Dept. Electrical Eng., University of Calgary


2009 - Advanced Data Analysis Methods
         Dept. Kinesiology, University of Calgary

Awards
BHSc 2008
University of Calgary Undergraduate Merit Award (2005)
Jason Lang Scholarship (2005)
Research Excellence Award, Student Symposium (2006)
Alberta Heritage Foundation Summer Studentship (2007)
O'Brien Center Conference Travel Award (2007)
Silver Medallion Bionformatics Univ. Calgary (2008)



MSc 2009 -
Alberta Heritage Foundation Studentship
TA - Introductory Cell Biology MDSC 408 (2)
Keith Cooper Award - Systems Neuroscience course
CIHR-CGS Banting and Best MSc Scholarship




PhD 2011 - April 2013
T. Chen Fong Award
CIHR-CGS Banting and Best PhD Studentship
Student Poster Award, Computational Neuroscience Meeting, Stockholm 2011
Dean's Publication and Mentorship Prize 2011
Izaak Walton Killam Scholarship
Honourable mention Poster Award, Computational Neuroscience Meeting, Atlanta 2012
Hotchkiss Brain Institute - PhD Student of the Year 2012
Research Focus: Synaptic activation of cerebellar Purkinje cells
Approach: I use patch clamp recordings in vitro to determine the relative contribution of calcium and potassium channels to synaptic responses in Purkinje cells
Preparations: In vitro slice preparation
Below are short summaries of my projects published from the lab.
Dual Recordings Purkinje cell Model - Cerebellar Purkinje cells
    I use patch clamp recording techniques to examine how voltage-gated potassium and calcium-dependent currents shape the firing properties of cerebellar Purkinje cells. The contribution of specific ion channels activated by synaptic inputs are analyzed using direct stimulation of afferent inputs or current commands to simulate the postsynaptic response.
CF discharge converts Purkinje cell output Climbing fiber input regulates intrinsic properties of Purkinje cells
    In this study we show that climbing fiber input activated at physiological frequencies blocks an intrinsic trimodal pattern inherent to Purkinje cells studied in vitro, restoring tonic Na+ spike discharge similar to that found in vivo. Moreover, all the effects of direct climbing fiber stimulation were reproduced by simulating climbing fiber input with an injected EPSC in the presence of synaptic blockers, emphasizing a key role for the postsynaptic complex spike depolarization in determining Purkinje cell activity. See McKay et al. 2007.
Firing dynamics of Purkinje cells Firing dynamics of cerebellar Purkinje cells
    We show that a simple firing model undergoing a saddle homoclinic bifurcation can reproduce many of the key properties of Purkinje cells. Each spike is followed by a relatively large depolarizing afterpotential (DAP) that can sustain tonic firing given a brief stimulation from rest. Consequently, within the context of a saddle homoclinic bifurcation the DAP is critical for bistable dynamics and many of the other electrophysiological characteristics of Purkinje cells. 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

IT and IH have distinct roles in DCN cell rebound responses 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 were 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
Cav3 T-type channels form a unique interaction with BK potassium channels T type calcium channels form a unique interaction with BK potassium channels
   Big conductance (BK) potassium channels complex with high voltage-activated calcium channels to interact at the nanodomain level. We now show that Cav3 T-type channels interact with the S0 segment of BK channels to evoke potassium current in the subthreshold range. An unexpected ability to block the interaction with internal EGTA is traced to a relatively weak calcium domain supported by Cav3 calcium influx, requiring multiple Cav3 channels to effect BK channel activation at the level of a microdomain. See Rehak et al. (2013). PDF
Modeling Cav3 and Cav3 interactions with KCa1.1 channels

Modeling Cav3 and Cav2 interactions with KCa1.1 channels
   A model of Cav calcium influx and BK channels provides a comparison of the relative ability for low voltage-activated Cav3 calcium channels or high voltage-activated Cav2.2 calcium channels to activate BK current. The model indicates that the low conductance and transient nature of calcium influx by Cav3 channels dictates the need for closer positioning, more calcium channels, and cooperative activity between Cav3-BK complexes to achieve comparable activation as Cav2.2 channels. See Engbers et al. (2013). 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).
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

McKay, B.E., Engbers, J.D.T., Mehaffey, W.H., Gordon, G., Molineux, M.L., Bains, J. and Turner, R.W. (2007) Climbing fiber discharge regulates cerebellar functions by controlling the intrinsic characteristics of Purkinje cell output. J. Neurophysiology
97: 2590-2604. PDF

Fernandez, F.R., Engbers, J.D.T. and Turner, R.W. (2007) Firing dynamics of cerebellar Purkinje cells. J. Neurophysiology 98(1): 278-94. PDF

Anderson, D.M., 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

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. Physiology (Lond.), 589 (Pt 22): 5391-413. * Shared first authors. PDF

Haitao Y., Tsutsui, S., Hameed, S., Kannanayakal, T.J., Chen, L., Peng, X., Engbers, J.D.T., Lipton,S.A., Stys, P. and Zamponi, G.W. (2012) Aβ neurotoxicity depends on interactions between copper ions, prion protein and N-methyl-D-aspartate receptors. PNAS 109 (5):1737-42.

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

Rehak, R., Bartoletti, T.M., Engbers, J.D.T., Berecki, G., Turner, R.W. and Zamponi, G.W. (2013)  Low voltage activation of KCa1.1 current by Cav3-KCa1.1 complexes. PLoS One 8 (4): e61844. PDF Top 25% in most cited articles, Jun 2017

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

Engbers, J.D.T., Zamponi, G.W., and Turner, R.W. (2013) Modeling interactions between voltage-gated calcium channels and KCa1.1. Channels 7(6). 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. * Shared first authors. Cell Reports. 11:1-8. Link

Dykstra, S., Engbers, J.D.T., Bartoletti, T.M. and Turner, R.W.  (2015) Determinants of rebound burst responses in rat cerebellar nuclear neurons to physiological stimuli. J. Physiology (Lond). 594(4): 985-1003.

Turner, R.W., Asmara, H., Engbers, J.D.T., Miclat, J., Rizwan, A.P., Sahu, G., and Zamponi, G.W. (2016) Assessing the role of IKCa channels in generating the slow AHP of CA1 hippocampal pyramidal cells. Channels 10(4): 313-319. Link

Asmara, H., Ileana M., Rizwan, A.P., Sahu, G., Simms, B.A., Zhang, F-X, Engbers, J.D.T., Stys, P.K., Zamponi, G.W., and Turner, R.W. (2017) A T-type channel-calmodulin complex triggers alpha-CaMKII activation, Molecular Brain,10:37. PDF.


Invited Chapters / Reviews

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., Fernandez, F.R. and Turner, R.W. (2012) Bistability in Purkinje neurons: ups and downs in cerebellar research. Special Issue: Computation in Cerebellum, In Neural Networks. ePub Sept 19.

Engbers, J.D.T. and Turner, R.W. (2013) Low voltage-activated calcium channels. In: Jaeger D., Jung R. (Ed.) Encyclopedia of Computational Neuroscience: Springer-Verlag Berlin Heidelberg.

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

Abstracts - Published work.

Engbers, J.D.T. Synaptic inputs are shaped by postsynaptic potassium channels in cerebellar Purkinje cells, Summer Student Symposium, University of Calgary 2006.

McKay, B.E., Engbers, J.D.T., Mehaffey, W.H., Gordon, G.R.J., Molineux, M.L., Bains, J.S. and Turner, R.W. Climbing fibre control of Purkinje cell spike output. Can Assoc Neurosci 2007 [Can J. Neurol. Sci., 34 (Supplement 3): S87].

Anderson, D.M., 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.M., 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 Cong. Neuroscience, 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., 2011. Prize, Student Poster Presentation.

Engbers, J.D.T., Turner, R.W. Cav3-KCa3.1 complex enhances detection of facilitating parallel fiber inputs in cerebellar Purkinje cells. Can. Assoc. Neurosci., 2012.

Engbers, J.D.T., Turner, R.W. Cav3-KCa3.1 complex enhances detection of facilitating parallel fiber inputs in cerebellar Purkinje cells. Comp. Neurosci., Honourable Mention, Student Poster Presentation, 2012.

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.

King, B., Teves, M., Seredynski, T., Kruskic, M., Asmara, H., Engbers, J.D.T., Hameed, S., Zamponi, G.W. and Turner, R.W. Expression pattern of the intermediate conductance Ca-activated K channel in the CNS. Can. Assoc. Neurosci., 2013.

Dykstra, S.N., Engbers, J.D.T., Bartoletti, T.M., Bosman, L.W.J, Owens, C.B., deZeeuw, C.I., and Turner, R.W. Deep cerebellar neurons differentially encode inhibitory inputs of Purkinje cells. Can. Assoc. Neurosci., 2013.

Engbers, J.D.T., Turner, R.W. Cav3-KCa3.1 complex enhances detection of facilitating parallel fiber inputs in cerebellar Purkinje cells. Can. Assoc. Neurosci., 2012.

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.

King, B., Teves, M., Seredynski, T., Kruskic, M., Asmara, H., Engbers, J.D.T., Hameed, S., Zamponi, G.W. and Turner, R.W.  Widespread expression of the intermediate conductance Ca-activated K channel in central neurons. Can. Assoc. Neurosci., 2013.

Bartoletti, T.M, Rehak, R., Engbers, J.D.T., Zamponi, G.W. and Turner R.W.  Low voltage activation of BK calcium-activated potassium channels by a novel complex with T-type calcium channels. 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.

King, B., Teves, M., Kruskic, M., Asmara, H., Engbers, J.D.T., Hameed, S., Zamponi, G.W. and Turner, R.W.  Widespread expression of the intermediate conductance Ca-activated K channel in central neurons.  Gordon Conference, Cerebellum, 2013.

Bartoletti, T.M., Rehak, R., Engbers, J.D.T., Zamponi, G.W. and Turner, R.W. A T-type-BK complex identified in medial vestibular neurons, Gordon Conference, Cerebellum 2013.

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