Michael B Robinson Ph.D.
Director, Analytical Neurochemistry and Spectroscopy CoreChildren's Hospital of Philadelphia, University of Pennsylvania
University of Pennsylvania
34th & Civic Center Boulevard
Abramson, Room 502D
Philadelphia, PA 19104
215-590-2205 (tel)
[email protected]
http://stokes.chop.edu/mrddrc/mrddrc.html
Biography/Curriculum Vitae:
Research Interests:
Neurobiology; excitatory neurotransmitter; excitotoxicity; brain injury
Narrative of Current Research Efforts:
Dr. Robinson is a neurobiologist interested in how the levels of a neurotransmitter, called glutamate, are controlled in the mammalian central nervous system. This amino acid is present at much higher levels (>1000-fold) than many other familiar neurotransmitters, such as serotonin, dopamine or acetylcholine. Glutamate is the predominant excitatory neurotransmitter and is required for essentially all sensory, motor, and cognitive function. In addition, appropriate glutamate signaling is required for normal brain development and memory formation. During an acute brain injury such as stroke or head trauma, glutamate is released from cells in abnormally high concentrations and excites cells to death. Dr. Robinson's research centers on understanding how the brain normally prevents this 'excitotoxicity' with the long range goal of developing novel strategies to prevent the injury that accompanies increased glutamate levels.
Dr. Robinson's laboratory is currently focusing on sodium-dependent high affinity transport systems that directly regulate the extracellular concentrations of amino acids. There are five members of a gene family that contribute to this activity. Using pharmacological, biochemical, physiological and molecular biological techniques, his research group is characterizing the transporters in both endogenous and heterologous expression systems. Dr. Robinson's team has been examining transcriptional, translational and post-translational regulation of these transporters in primary cultures of neurons and astrocytes and in cell lines that endogenously express these transporters. They have demonstrated that at least two of the transporters can be regulated by changing their cell surface distribution and that these effects are associated with a variety of protein-protein interactions.
Major Honors and Awards:
- Regulation of Extracellular Excitotoxins - National Institutes of Health
- Glutamate Transporters in the CNS - National Institutes of Health
- Enhancing and Expanding Research Projects in Mental Retardation - The Philadelphia Foundation
- Trafficking of a Neuronal Glutamate Transporter, EAAC1 - National Institutes of Health
Representative Publications:
Gonzalez MI, Robinson MB.; Protein KINASE C-Dependent Remodeling of Glutamate Transporter Function. Mol Interv. 2004 Feb;4(1):48-58.
Fournier KM, Gonzalez MI, Robinson MB.; Rapid trafficking of the neuronal glutamate transporter, EAAC1: evidence for distinct trafficking pathways differentially regulated by protein kinase C and platelet-derived growth factor. J Biol Chem. 2004 Aug 13;279(33):34505-13.
Kalandadze A, Wu Y, Fournier K, Robinson MB.; Identification of motifs involved in endoplasmic reticulum retention-forward trafficking of the GLT-1 subtype of glutamate transporter. J Neurosci. 2004 Jun 2;24(22):5183-92.
Created 1/4/2006 by Evette Mezger
Last modified 1/10/2023 by Oksana Klimova
