Matthew N. Rasband

Role of neuronal-glial signaling in brain development, function, injury and disease

Our long range goals are to elucidate the processes that underlie the molecular assembly of electrogenic compartments of axons and the role that myelinating cells (oligodendrocytes and Schwann cells) play in this process in health and in disease. Our lab explores the molecular basis of signaling between glial cells and axons in the brain and spinal cord under a variety of conditions including the normal process of myelination that occurs during development, demyelination and remyelination in disorders such as multiple sclerosis and the responses of axons and their myelinating cells to injuries of various types, including trauma. Our laboratory is working to understand the underlying mechanisms that regulate the clustering of ion channels at the sites that initiate and propagate action potentials: the axon initial segment and nodes of Ranvier. Many nervous system diseases and injuries result in the disruption of these domains. For example, traumatic brain and spinal cord injury (TBI and SCI), as well as demyelinating diseases like multiple sclerosis result in widespread axonal injury. It is now appreciated that a host of molecular events occurs that ultimately results in the disruption of axons and their excitable domains. One particularly sensitive component of axons is the spectrin/ankyrin based cytoskeleton. Spectrins and ankyrins are highly enriched at axon initial segments and nodes of Ranvier and are essential for maintaining both the high-density cluster of ion channels. Our research team is working to uncover the molecular mechanisms regulating formation and maintenance of ion channel clusters in axons since any therapeutic strategy aimed at nervous system repair and/or regeneration will require the re-establishment of these excitable domains.

Selected Publications

Boiko T, Rasband MN, Levinson SR, Caldwell JH, Mandel G, Trimmer JS, Matthews G (2001) Compact myelin dictates the differential targeting of two sodium channel isoforms in the same axon. Neuron 30:91-104.

Rasband MN, Park EW, Vanderah TW, Lai J, Porreca F, Trimmer JS (2001) Distinct potassium channels on pain-sensing neurons. Proceedings of the National Academy of Sciences USA 98:13373-13378.

Schafer DP, Bansal R, Hedstrom KL, Pfeiffer SE, Rasband MN (2004) Does paranode formation and maintenance require partitioning of neurofascin 155 into lipid rafts? Journal of Neuroscience 24:3176-3185.

Yang Y, Lacas-Gervais S, Morest DK, Solimena M, Rasband MN (2004) βIV spectrins are essential for membrane stability and the molecular organization of nodes of Ranvier. Journal of Neuroscience 24:7230-7240.

Ogawa Y, Schafer DP, Horresh I, Bar V, Hales K, Yang Y, Susuki K, Peles E, Stankewich MC, Rasband MN (2006) Spectrins and ankyrinB constitute a specialized paranodal cytoskeleton. Journal of Neuroscience 26:5230-5239.

Schafer DP, Custer AW, Shrager P, Rasband MN (2006) Early events in node of Ranvier formation during myelination and remyelination in the PNS. Neuron Glia Biology 2:69-79.

Schafer DP, Rasband MN (2006) Glial regulation of the axonal membrane at nodes of Ranvier. Current Opinion in Neurobiology 16:508-514.

Yang Y, Ogawa Y, Hedstrom KL, Rasband MN (2007) βIV spectrin is recruited to axon initial segments and nodes of Ranvier by ankyrinG. Journal of Cell Biology 176:509-519.

Spiegel I, Adamsky K, Eshed Y, Milo R, Sabanay H, Sarig-Nadir O, Horresh I, Scherer SS, Rasband MN, Peles E (2007) A central role for Necl4 (SynCAM4) in Schwann cell-axon interaction and myelination. Nature Neuroscience 10:861-869.

Hedstrom KL, Xu X, Ogawa Y, Frischknecht R, Seidenbecher CI, Shrager P, Rasband MN (2007) Neurofascin assembles a specialized extracellular matrix at the axon initial segment. Journal of Cell Biology 178:875-886.

Contact Information

Matthew N. Rasband, Ph.D.

Department of Neuroscience

Baylor College of Medicine

One Baylor Plaza,

Houston, Texas 77030, U.S.A.

Tel: (713) 798-4494

Fax: (713) 798-3946

E-mail: rasband@bcm.edu