Keith K. Murai

ORCID: 0000-0002-5313-1106
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Axon Guidance and Neuronal Signaling
  • Photoreceptor and optogenetics research
  • Alzheimer's disease research and treatments
  • Genetics and Neurodevelopmental Disorders
  • Nerve injury and regeneration
  • Memory and Neural Mechanisms
  • Mitochondrial Function and Pathology
  • Zebrafish Biomedical Research Applications
  • RNA regulation and disease
  • Single-cell and spatial transcriptomics
  • Signaling Pathways in Disease
  • Amino Acid Enzymes and Metabolism
  • Neuroscience and Neural Engineering
  • MicroRNA in disease regulation
  • Immune cells in cancer
  • Barrier Structure and Function Studies
  • Bone and Dental Protein Studies
  • Systemic Sclerosis and Related Diseases
  • Neurobiology and Insect Physiology Research
  • Cerebral Venous Sinus Thrombosis
  • Nuclear Receptors and Signaling
  • Down syndrome and intellectual disability research

McGill University Health Centre
2016-2025

Montreal General Hospital
2016-2025

McGill University
2010-2025

Princip (Czechia)
2019

Sanford Burnham Prebys Medical Discovery Institute
1999-2012

University of California, San Diego
1997-2002

The injured adult mammalian spinal cord shows little spontaneous recovery after injury. In the present study, contribution of projections in dorsal half to functional loss injury was examined, together with effects transgenic cellular delivery neurotrophin-3 (NT-3) on morphological and disturbances. Adult rats underwent bilateral column lesions that remove corticospinal or more extensive resections entire bilaterally corticospinal, rubrospinal, cerulospinal projections. Long-lasting deficits...

10.1523/jneurosci.17-14-05560.1997 article EN cc-by-nc-sa Journal of Neuroscience 1997-07-15

Accumulating evidence is redefining the importance of neuron–glial interactions at synapses in CNS. Astrocytes form “tripartite” complexes with presynaptic and postsynaptic structures regulate synaptic transmission plasticity. Despite our understanding relationships physiological contexts, little known about structural interplay between astrocytes synapses. In past, this has been difficult to explore because studies have hampered by lack a system that preserves complex observed brain. Here...

10.1523/jneurosci.1302-06.2006 article EN cc-by-nc-sa Journal of Neuroscience 2006-08-30

Glial cell properties dictated by neurons Neurons in the brain coexist with astrocytes, a type of glial cell, which help support many functions their neighboring nerve cells. Farmer et al. now show that goes both ways (see Perspective Stevens and Muthukumar). They explored influence on two specialized types astrocytes mouse cerebellar cortex. The produced morphogen known as Sonic Hedgehog. Hedgehog signaling adjusted distinctive gene expression within astrocyte types. Thus, mature appear to...

10.1126/science.aab3103 article EN Science 2016-02-19

Increasing evidence indicates the importance of neuron-glia communication for synaptic function, but mechanisms involved are not fully understood. We reported that EphA4 receptor tyrosine kinase is in dendritic spines pyramidal neurons adult hippocampus and regulates spine morphology. now show ephrin-A3 ligand, which located perisynaptic processes astrocytes, essential maintaining activation normal morphology vivo. Ephrin-A3-knockout mice have irregularities similar to those observed...

10.1073/pnas.0903328106 article EN Proceedings of the National Academy of Sciences 2009-07-11

The transmembrane protein deleted in colorectal cancer (DCC) and its ligand, netrin-1, regulate synaptogenesis during development, but their function the mature central nervous system is unknown. Given that DCC promotes cell-cell adhesion, expressed by neurons, activates proteins signal at synapses, we hypothesized expression neurons regulates synaptic plasticity adult brain. We report enriched dendritic spines of pyramidal wild-type mice, demonstrate selective deletion from forebrain...

10.1016/j.celrep.2012.12.005 article EN cc-by Cell Reports 2013-01-01

Neurons recruit numerous mechanisms to facilitate the development of synaptic connections. However, little is known about activity-dependent that control timing and fidelity this process. Here we describe a novel pathway used by neurons regulate glutamate receptors at maturing central synapses. This relies on communication between astrocytes ability release factor SPARC (secreted protein, acidic rich in cysteine). expression dynamically regulated plays critical role determining level AMPARs....

10.1523/jneurosci.4757-10.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-03-16

Remodeling of dendritic spines is believed to modulate the function excitatory synapses. We previously reported that EphA4 receptor tyrosine kinase regulates spine morphology in hippocampal pyramidal neurons, but signaling pathways involved were not characterized (Murai, K.K., L.N. Nguyen, F. Irie, Y. Yamaguchi, and E.B. Pasquale. 2003. Nat. Neurosci. 6:153-160). In this study, we show activation by ephrin-A3 slices inhibits integrin downstream pathways. decreases phosphorylation scaffolding...

10.1083/jcb.200610139 article EN The Journal of Cell Biology 2007-09-17

Abstract Fixed human brain samples in tissue repositories hold great potential for unlocking complexities of the and its alteration with disease. However, current methodology simultaneously resolving complex three-dimensional (3D) cellular anatomy organization, as well as, intricate details cells has been limited due to weak labeling characteristics high background levels. To expose these samples, we developed a method overcome major limitations. This approach offers an unprecedented view...

10.1038/srep24544 article EN cc-by Scientific Reports 2016-04-19

Abstract Epileptogenesis is the gradual process by which healthy brain develops epilepsy. However, neuronal circuit changes that underlie epileptogenesis are not well understood. Unfortunately, current chemically or electrically induced epilepsy models suffer from lack of cell specificity, so it seldom known cells were activated during epileptogenesis. We therefore sought to develop an optogenetic variant classical kindling model in activatable both genetically defined and fluorescently...

10.1038/s41598-019-41533-2 article EN cc-by Scientific Reports 2019-03-27
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