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| Thanks to the following for materials & support |
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Neural Diseases
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Collaborative interests have extended beyond the usual neuronal perspectives to include that of the glial component of the brain, in particular the microglia key players in brain function as well as in Alzheimer's plaque formation. Studies of reactive species, such as nitric oxide and hydrogen peroxide, as well as oxygen consumption, have produced particularly interesting results.
The advent of miniaturized, non-invasive and rapid response oxygen sensors operating in a modulation or self-referencing format has opened up single neuron metabolism to our investigation. Driven by collaborative demand we are now examining through electrochemistry, imaging and photon detection, the mitochondrial changes induced by the anti-apoptotic protein Bcl-xl. This protein is induced within neurons in response to stroke and ischemia. It also appears in the heart during oxidative stress.
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| A heterogeneous coculture of neural cells. The neurites of three hippocampal neurons (green; neuronal βIII tubulin) are clearly visible within a myriad of glial cells (yellow; glial fibrillary acidic protein) and fibroblasts. Glia and fibroblasts support and direct the growth of neurons. Mitochondria (red; Mitotracker) and nuclei (blue; DAPI) are shown. |
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• Neuronal glucose detection & hypoglycemia-associated
autonomic failure >> |
| • Glutamate excitotoxicity >> |
| • Mitochondrial channel activity within a living synapse >> |
| • Effects of hyperglycemia on living mouse embryos >> |
| • Synergistic amplification of beta-amyloid & infgamma-induced microglial >> |
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| Twig, G., Graf, S.A., Messerli, M.A., Smith, P.J.S., Yoo, S.H., Shirihai, O.S. 2005. Synergistic amplification of beta-amyloid- and interferon-gamma-induced microglial neurotoxic response by the senile plaque component chromogranin A. American Journal of Physiology-Cell Physiology, 288:C169-C175. |
| Kumar, S.M., Porterfield, D.M., Muller, K.J., Smith, P.J. and Sahley, C.L. 2001. Nerve injury induces a rapid efflux of Nitric Oxide (NO) detected with a novel NO microsensor. Journal of Neuroscience. 21(1): 215-220. |
| Twig, G., Jung, S.-K., Messerli, M., Smith, P.J.S. and Shirihai, O. 2001. Real-time detection of reactive oxygen intermediates from single microglial cells. Biological Bulletin, 201(2): 261-262. |
| DeTrait, E., Eddleman, C.S., Yoo, S.M., Fukuda, M., Nguyen, M.P., Bittner, G.D. and Fishman, H.M. 2000. Axolemmal repair requires proteins that mediate synaptic vesicle fusion. Journal of Neurobiology, 44: 382-391. |
| Eddleman, C.S., Bittner, G.D. and Fishman, H.M. 2000. Barrier permeability at cut axonal ends progressively decreases until an ionic seal is formed. Biophysical Journal, 79: 1883-1890. |
| Shirihai, O., Smith, P.J.S., Hammar, K. and Dagan, D. 1998. H+ and K+ gradient generated by microglia H/K ATPase. Glia 23: 339-348. |
| Eddleman, C.S., Ballinger, M.L., Smyers, M.E., Fishman, H.M. and Bittner, G.D. 1998. Endocytotic formation of vesicles and other membranous structures induced by Ca2+ and injury. Journal of Neuroscience, 18(11): 4029-4041. |
| Eddleman, C.S., Smyers, M.E., Lore, A., Fishman, H.M. and Bittner, G.D. 1998. Anomalies associated with dye exclusion as a measure of axolemmal repair in invertebrate axons. Neuroscience Letters, 256(3): 123-126. |
| Eddleman, C.S., Ballinger, M.L., Godell, C.M., Smyers, M.S., Fishman, H.M. and Bittner, G.D. 1997. Repair of plasmalemmal lesions by vesicles. Proceedings of the National Academy of Sciences, 94: 4745-4750. |
| Godell, C.M., Smyers, M.S., Eddleman, C.S., Ballinger, M.L., Fishman, H.M. and Bittner, G.D. 1997. Calpain activity promotes sealing of severed giant axons. Proceedings of the National Academy of Sciences, 94: 4751-4756. |
| Knox, R.J., Kao, L.S., Jonas, E., Smith, P.J.S., Connor, J.A. and Kaczmarek, L.K. 1996. Ca2+ influx and activation of a cation current are coupled to an intracellular Ca2+ mobilization of peptidergic neurons. Journal of Physiology, 494(3): 627-639. |
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Equipment
