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Arsalan Pervaiz

Arsalan Rizwan,  BSc Biochem, Univ Calgary
PhD Student,
Dept. Neuroscience, 2016

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
arpervai@ucalgary.ca

Training
BSc 2012
University of Calgary
Alberta Canada



Awards
BSc
2010 Markin Summer Studentship
2011 AIHS Summer Studentship
2010-2012 Jason Lang Scholarship


MSc 2012 -
Queen Elizabeth II Award, MSc, Dept. Neuroscience
HBI Education Committee Travel Award CAN 2013
TAship, Cellular and Molecular Neuroscience
Top Presentation Award, Student Research Day 2014

PhD 2016
Dept. Neuroscience Travel Award
Queen Elizabeth II Award, PhD, Dept. Neuroscience
Medical School admission 2016, Queen's University
Poster Award, Hotchkiss Brain Research Day
Alberta Innovates-Health Solutions Studentship
HBI Trainee Publication Award
HBI PhD Student of the Year - Runner up 2016
Brain Star Award, CIHR Inst Neurosci., Mental Health and Addiction

Research Focus: The mechanisms and role of a Cav3-Kv4 ion channel complex
Approach: I use patch clamp recordings in vitro to determine the ability for a novel Cav3-Kv4 complex to control neuronal excitability in cerebellar neurons
Preparations: In vitro slice preparation, optogenetics, voltage clamp
Below are short summaries of my projects published from the lab.
KChiP3 mediated shift in Kv4 inactivation selectively modulates signal processing in lobule 9 granule cells

Model - Cav3-Kv4 interaction
    A-type potassium channels of the Kv4 family regulate the latency and frequency of spike output in numerous CNS cells. T-type calcium channels of the Cav3 family share many of the properties of A-type potassium channels, and in fact link at the molecular level to provide calcium-dependent regulation of A-type current. I use patch clamp recordings to assess how this novel ion channel complex regulates spike output and signal processing in cerebellar granule cells.

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)).
A Mossy fiber LTP reduces IA to potentiate burst output from cerebellar granule cells

Long-term potentiation at the mossy fiber-granule cell relay
   Short bursts of mossy fiber synaptic inputs to cerebellar granule cells signal the occurrence of meaningful sensory input from the periphery and can exhibit long-term potentiation. This study identified a dramatic increase in postsynaptic excitability due to a shift in the voltage-dependence of Kv4 potassium channels that reduces A-type current in granule cells. The shift in Kv4 properties depends on coactivation of mGlu and NMDA receptors and ERK-mediated kinase activity, with a selective potentiation of burst output from granule cells. See Rizwan et al. 2016.

Peer-reviewed Publications

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

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

Rizwan, A.P., Zhan, X., Zamponi, G.W. and Turner, R.W. (2016) Long-term potentiation at the mossy fiber-granule cell relay invokes postsynaptic second messenger regulation of Kv4 channels. J. Neuroscience 36(44): 11196-11207.

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.

Abstracts

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.

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.


Rizwan, A.P., Zamponi, G.W. and Turner, R.W.  Role of the Cav3-Kv4 complex in mediating synaptic learning in cerebellar granule cells.  Can. Assoc. Neurosci., 2014.

Rizwan, A.P., Zamponi, G.W. and Turner, R.W. Dynamic synaptic regulation of IA in granule cells of the cerebellum. Proc. Soc. Neurosci., 2014.

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. IKCa channels are a critical determinant of the slow AHP in CA1 hippocampal pyramidal cells.  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.

Rizwan, A.P., Zamponi, G.W. and Turner, R.W. NMDAR-induced plasticity of A-type Kv4 current contributes to long-term potentiation of mossy fiber input in granule cells of posterior cerebellum. Proc. Soc. Neurosci., 2015.

Rizwan, A.P., Zhan, X., Zamponi, G.W. and Turner, R.W. Long-term potentiation in cerebellar granule cells modifies Kv4 channel A-type current. Fed. Eur. Neurosci., 2016.

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