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X Zhan
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Xiaoqin Zhan

Xiaoqin Zhan Postdoctoral Fellow    
BSc Bioengineering, Shanghai University, China 2008
PhD Biophysics & Neuroscience, Fudan University, China 2013
PhD Dissertation: Development of cerebellar granule cells

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

Training / Experience
2008 - 2013
PhD Molecular Pharmacology & Cellular Signaling
Fudan University
Supervisor: Professor Yan-ai Mei

2013 - 2015
Group Leader
Wolwo Biotech Pharma Co.
Shanghai, China

2016 -
University of Calgary
Calgary Alberta
Supervisor: Dr. R.W. Turner
National Scholarship - Ministry of Education of China, 2005


Xianghui Acadamic Scholarship in Fudan University, 2010
Excellent Graduates in Fudan University, 2013

Hotchkiss Brain Institute Postdoctoral Fellowship
Cumming School of Medicine Postdoctoral Scholarship

Workshop - Computational Neuroscience, Univ. Lethbridge, June 2016

Research Focus: Cav3-Kv4 interactions in cerebellum
Approach: Electrophysiology in vitro, molecular biology, pharmacology
Preparations: Expression systems, in vitro slice preparations
Below are short summaries of my publications.

PhD Thesis research:
My PhD work centered on ion channels that regulate cerebellar granule cell development

Electromagnetic fields and sodium channels
In this study, we examined the sodium current in cerebellar granule cells after exposure to extremely low frequency electromagnetic fields (ELF-EMF) using whole-cell patch recording. We found that ELF-EMF exposure increased the sodium current density and altered the biophysical properties of  sodium channels, mainly Nav1.2, by activating the cAMP/PKA pathway.
GABAA receptor subunit expression and cerebellar granule cell maturation
In this work, we compared the morphology of cerebellum in APP knockout and wildtype mice, and found that amyloid peptide (Aβ) is involved in the maturation of cerebellum and increased the expression of the GABAA receptor α6 subunit. This regulation is ERK-mTOR pathway-dependent through activating the p75 receptor.
Citalopram inhibits delayed rectifier potassium current
In this study, we examined the block of delayed rectifier voltage-dependent potassium current (Ik) in cortical neurons and HEK 293 cells by the antidepressant citalopram. We found that citalopram evoked a concentration-dependent inhibition of Ik  (Kv2.2). Citalopram acts by left shifting the steady-state activation and inactivation profiles, increasing action potential duration and firing properties of cortical neurons.
Neuritin up-regulates Kv4.2-mediated potassium current
In this study, we examined the effect of Neuritin, a new neurotrophic factor, on voltage-dependent potassium channels and the involved receptor and downstream signal effectors. We found neuritin specifically increases the density of transient potassium current (IA) by binding to the insulin receptor and activating the ERK, Akt and mTOR signals.
Amoxapine inhibits the delayed rectifier outward K+ current in cortical neurons
In this study, we examined the inhibition of delayed rectifier K+ current (Ik) by the antidepressant Amoxapine. Amoxapine concentration dependently decreased Ik  (Kv2.1) by modulating the steady-state activation and inactivation properties. Immunostaining and signal activator and inhibitor results suggest that this regulation is PKA/cAMP pathway-dependent and involves 5-HT receptors.

Postdoctoral research:
My work is focused on the interaction between Cav3 T-type calcium channels and Kv4 A-type potassium channels.

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 link at the molecular level to provide calcium-dependent regulation of A-type current. I use patch clamp recordings to assess the structure-function of this novel ion channel complex and how it regulates signal processing in cerebellar granule cells.

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

He YL, Liu DD, Fang YG, Zhan XQ, Yao JJ, Mei YA. (2016) Exposure to Extremely Low-Frequency Electromagnetic Fields Modulates Na+ Currents in Rat Cerebellar Granule Cells through Increase of AA/PGE2 and EP Receptor-Mediated cAMP/PKA Pathway. PLoS ONE 8(1): e54376.

Zhan XQ
, Yao JJ, Liu DD, Ma Q, Mei YA. (2014) Aβ40 modulates GABAA receptor α6 subunit expression and rat cerebellar granule neuron maturation through the ERK/mTOR pathway. J. Neurochemistry 128 (3): 350-362.

Zhan XQ
, He YL, Yao JJ, Zhuang JL, Mei YA. (2012) The antidepressant citalopram inhibits delayed rectifier outward K⁺ current in mouse cortical neurons. J. Neuroscience Res. 90 (1): 324-336.

Yao JJ, Gao XF, Chow CW, Zhan XQ, Hu CL, Mei YA. (2012) Neuritin Activates Insulin Receptor Pathway to Up-regulate Kv4.2-mediated Transient Outward K+ Current in Rat Cerebellar Granule Neurons. J. Biological Chemistry 287 (49): 41534-41545.

He YL, Zhan XQ, Yang G, Sun J, Mei YA. (2010) Amoxapine inhibits the delayed rectifier outward K+ current in mouse cortical neurons via cAMP/protein kinase A pathways. J. Pharmacol. Exp. Ther. 332 (2) :437-445.

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.

Key Abstracts

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.

Xiao-Qin Zhan, Yan-Lin HE, Jin-Jing YAO, Jia-Li ZHUANG,Yan-Ai MEI. Antidepressant citalopram inhibits Kv2.1 in mouse cortical neurons. The 9th Meeting Chinese Society for Neuroscience. Zhengzhou, China. 2011.

Xiao-Qin Zhan, Yan-Lin He. Antidepressant citalopram directly inhibits delayed rectifier potassium channel in cortical neurons. Can. Assoc. Neuroscience, Ottawa, Canada, 2010.

Xiao-Qin Zhan, Yan-Lin He, Jin-Jing Yao, Jia-Li Zhuang, Yan-Ai Mei. Antidepressant drug citalopram inhibits delayed rectifier outward K+ current in mouse cortical neurons. The 4th Shanghai International Conference on Biophysics and Molecular Biology, Shanghai, China, 2010.

Yan-Lin He, Xiao-Qin Zhan, Yan-ai Mei. The mechanism in Amoxapine inhibiting IK current in cortical neurons. The 11th Chinese Biophysics Conference. Guilin, China, 2009.

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