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| |  John Barrett, Ph.D. Professor, Physiology and Biophysics 305-243-6357 (office) 305-243-5931 (fax) Rosenstiel Medical Science Building - 5018A jbarrett@med.miami.edu
- 1965 B.A. Biology, Chemistry, Mathematics summa cum laude, St. Mary's College, Winona MN
- 1972 Ph.D. Physiology and Biophysics, University of Washington, Seattle WA
- 1972-1973 Research Associate, Anatomy, University of Colorado, Denver CO
- 1973-1974 Postdoctoral Fellow, Neurobiology, Harvard Medical School and University of Iowa
- 1974-1978 Assistant Professor, Dept. of Physiology and Biophysics, University of Miami School of Medicine
- 1978-1985 Associate Professor, Dept. of Physiology and Biophysics, University of Miami School of Medicine
- 1985-present Professor, Dept. of Physiology and Biophysics, University of Miami School of Medicine
- 1986-1993 Javits Neuroscience Investigator Award
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Our laboratory studies how mammalian central neurons respond to environmental stresses. One project seeks to determine mechanisms underlying the complementary neuroprotective effects of neurotrophins (e.g. NGF, BDNF) and certain bone morphogenetic proteins (e.g. BMP7) during hypoglycemic stress. This project focusses on septal neurons, especially the cholinergic population. Another project studies mechanisms by which striatal and septal neurons respond to hyperthermia, including why hyperthermia exacerbates the damage produced by other stresses such as hypoglycemia and ischemia. Our current work focusses on cultured neurons, but we are beginning to incorporate in vivo approaches as well. Knowledge concerning the dominant mechanisms underlying stress-induced neuronal damage will aid in designing strategies to minimize the delayed neuronal death that follows these stresses.
Techniques used in my laboratory include cell culture of mammalian neurons, fluorescence and confocal videomicroscopy, use of fluorescent indicators for e.g. Ca2+ and mitochondrial function, assays for cell survival and transmitter synthesis, immunohistochemistry, PCR, Western blots, and transfection with cDNA for mutant or fluorescent proteins involved in intracellular signalling.
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Nguyen KT, Barrett, JN, García-Chacón LE, David G, Barrett, EF. Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice. Neurobiology of Disease, 2011, epub Feb. 17.
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Chaverneff F, Barrett JN (2009). Casein kinase II contributes to the synergistic effects of BMP7 and BDNF on Smad 1/5/8 phosphorylation in septal neurons under hypoglycemic stress. J Neurochem, 2009; 109(3):733-743 epub Feb. 13.
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Nguyen KT, García-Chacón LE, Barrett JN, Barrett EF, David G. (2009) The Ψm depolarization that accompanies mitochondrial Ca2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals. Proc Natl Acad Sci USA, 2009; 106(6):2007-2011, epub Jan 27
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- White MG, Luca LE, Nonner D, Saleh O, Hu B, Barrett EF, Barrett JN. Cellular mechanisms of neuronal damage from hyperthermia.Prog Brain Res. 2007;162:347-71. Review.
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- Nonner D, Panickar K, Barrett EF, Barrett JN. (2004) Bone morphogenetic proteins and neurotrophins provide complementary protection of septal cholinergic function during phosphatase inhibitor-induced stress. Journal of Neurochem 2004; 91:77-87.
- White MG, Emery M, Nonner D, Barrett JN (2003) Caspase activation contributes to delayed death of heat-stresed striatal neurons. Journal of Neurochem 2003, 87:958-968.
- Nonner D, Barrett EF, Kaplan P, Barrett JN (2001) Bone morphogenetic proteins (BMP6 and BMP7) enhance the protective effect of neurotrophins on cultured septal cholinergic neurons during hypoglycemia. Journal of Neurochemistry 76:1-10.
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