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Dr. Lyanne Schlichter - University Health Network. Toronto, ON, CA

Dr. Lyanne Schlichter Dr. Lyanne Schlichter

Senior Scientist | University Health Network

Toronto, ON, CANADA

Dr. Lyanne Schlichter is a Senior Scientist at Krembil with interests in neuroimmunology, ion-channel regulation, and cancer.





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Lyanne C. Schlichter is a Senior Scientist at Krembil Research Institute (Krembil) with research interests in neuroimmunology, ion-channel regulation, and cancer. She is also a Professor in the Department of Physiology, University of Toronto.

Lyanne C. Schlichter's laboratory focuses on neuroinflammation and comprises 3 main research topics. Experimental approaches range from in vivo models → cell cultures → molecules. Current projects combine two or more principle techniques. She has published many seminal papers on microglia, ion channels, and in vivo studies of inflammation and CNS damage. The lab has been continually well-supported by grants from national granting agencies (CIHR, Heart & Stroke Foundation, Canadian Stroke Network, NSERC), as well as scholarships and fellowships.

Industry Expertise (3)


Health Care - Services


Areas of Expertise (10)





Cell Physiology

Molecular Biology


Stroke Treatment


University Teaching

Media Appearances (1)

Brain Inflammation: Harmful or Helpful?

The Brain Campaign  online


There are many qualities of Schlichter’s work that make it unique from other labs studying stroke ...

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Articles (5)

After Intracerebral Hemorrhage, Oligodendrocyte Precursors Proliferate and Differentiate Inside White-Matter Tracts in the Rat Striatum Translational Stroke Research


Damage to myelinated axons contributes to neurological deficits after acute CNS injury, including ischemic and hemorrhagic stroke. Potential treatments to promote re-myelination will require fully differentiated oligodendrocytes, but almost nothing is known about their fate following intracerebral hemorrhage (ICH). Using a rat model of ICH in the striatum, we quantified survival, proliferation, and differentiation of oligodendrocyte precursor cells (OPCs) (at 1, 3, 7, 14, and 28 days) in the peri-hematoma region, surrounding striatum, and contralateral striatum.

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Expression and contributions of the Kir2.1 inward-rectifier K(+) channel to proliferation, migration and chemotaxis of microglia in unstimulated and anti-inflammatory states Frontiers in Cellular Neuroscience


When microglia respond to CNS damage, they can range from pro-inflammatory (classical, M1) to anti-inflammatory, alternative (M2) and acquired deactivation states. It is important to determine how microglial functions are affected by these activation states, and to identify molecules that regulate their behavior. Microglial proliferation and migration are crucial during development and following damage in the adult, and both functions are Ca(2+)-dependent.

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PKA reduces the rat and human KCa3.1 current, CaM binding, and Ca2+ signaling, which requires Ser332/334 in the CaM-binding C terminus The Journal of Neuroscience


he Ca(2+)-dependent K(+) channel, KCa3.1 (KCNN4/IK/SK4), is widely expressed and contributes to cell functions that include volume regulation, migration, membrane potential, and excitability. KCa3.1 is now considered a therapeutic target for several diseases, including CNS disorders involving microglial activation; thus, we need to understand how KCa3.1 function is regulated. KCa3.1 gating and trafficking require calmodulin binding to the two ends of the CaM-binding domain (CaMBD), which also contains three conserved sites for Ser/Thr kinases.

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Expression and contributions of TRPM7 and KCa2.3/SK3 channels to the increased migration and invasion of microglia in anti-inflammatory activation states PLoS One


Microglia rapidly respond to CNS injury and disease and can assume a spectrum of activation states. While changes in gene expression and production of inflammatory mediators have been extensively described after classical (LPS-induced) and alternative (IL4-induced) microglial activation, less is known about acquired de-activation in response to IL10. It is important to understand how microglial activation states affect their migration and invasion; crucial functions after injury and in the developing CNS. We reported that LPS-treated rat microglia migrate very poorly, while IL4-treated cells migrate and invade much better.

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The microglial activation state regulates migration and roles of matrix-dissolving enzymes for invasion Journal of Neuroinflammation


Microglial cells are highly mobile under many circumstances and, after central nervous system (CNS) damage, they must contend with the dense extracellular matrix (ECM) in order to reach their target sites. In response to damage or disease, microglia undergo complex activation processes that can be modulated by environmental cues and culminate in either detrimental or beneficial outcomes. Thus, there is considerable interest in comparing their pro-inflammatory ('classical' activation) and resolving 'alternative' activation states. Almost nothing is known about how these activation states affect the ability of microglia to migrate and degrade ECM, or the enzymes used for substrate degradation. This is the subject of the present study.

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