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EDUCATION:
B.S.University of Missouri 1963 Electrical Engineering
M.S.Northwestern University 1964 Electrical (Biomedical) Engineering
Ph.D Northwestern University 1967 Electrical (Biomedical) Engineering
PROFESSIONAL EXPERIENCE:
1989-1995
Head, Department of Neurosciences / Member, Executive Board
Roche Institute of Molecular Biology
Hoffman LaRoche Research Center
Nutley, N.J. 07110
1981 -
1989 Member , Distinguished Member of Technical Staff
Molecular Biophysics Research Department
Bell Laboratories, AT&T Bell Laboratories
Murray Hill, New Jersey 07971
1969 -
1981 Assistant, Associate, Full Professor
Department of Physiology and Biophysics
University of Illinois
Urbana, Illinois 61820
1967 -
1969 Research Associate
Department of Physiology and Biophysics
University of Washington
Seattle, Washington 98195
PROFESSIONAL
SOCIETIES HONORARY SOCIETIES AND AWARDS
Society for Neuroscience
Camillo Golgi Award, from FIDIA Research Foundation (1991)
Biophysical Society
Distinguished Member of Technical Staff: Bell Laboratories (1987)
The Harvey Society
Grass Foundation Summer Fellowship (1971)
Editorial Boards
Present: Learning and Memory , J. Neurophysiol., Biophys. J.
Past: NeuroImage, Cell and Molecular Neurobiology, Am. J. Physiol.,
Cell Calcium
RESEARCH
INTERESTS
Studies are directed at discovering the means by which electrical signals
in nerve cells of the brain are coupled to the biochemistry that produces long
lasting changes in neuron excitability. In some instances these may be
the cellular mechanisms of memory. Interest centers around intracellular
free calcium (Ca2+) as the primary trigger mechanism for these memory
mechanisms. This general area of study also has strong bearing on the
origins of pathological states arising from such things as stroke (acute ischemic
damage) or longer-term, more subtle damages to neurons such as may occur in
eplepsy or the numerous forms of dementia. These pathological states may
well be the result of otherwise normal processes involved in learning and memory
being thrown out of control by physically or chemically induced trauma.
The laboratory uses biophysical methods to examine the chemical and electrical
events at the level of single nerve cells. These techniques include digital
imaging of fluorescent molecules that report changes in the concentrations of
Ca2+ or the pH in these small volumes, and patch clamping where the
electrical currents in single cells are measured. The former technique
allows one to see a nerve cell or one of its connections to another cell respond
to a chemical (neurotransmitter) or electrical signal.
REPRESENTATIVE PUBLICATIONS
Connor, J.A. and Shuttleworth, C.W.R. Intracellular Ca2+ Signals Underlying Rapid and Delayed Excitotoxicity in Mature CNS Neurons. In: New Concepts in Cerebral Ischemia. Ed. R. C.S. Lin. CRC Press. Chapt. 5 pp11-133 (2002).
Golarai, G., Greenwood, A.C., Feeney, D.M., & Connor, J.A. Physiological and structural evidence for hippocampal in persistent seizure susceptibility after traumatic brain injury. J. Neurosci. 21:8523-8537 (2001).
Zou, B., Golarai, G, Connor, J.A., & Tang, A.C. Neonatal exposure to a novel environment enhances the effects of corticosterone on neuronal excitability and plasticity in adult hippocampus. Br. Res. 130:1-7 (2001).
Shuttleworth, C.W.R. and Connor, J.A. Strain-Dependent differences in calcium signaling predict excitotoxicity in murine hippocampal neurons. J. Neurosci. 21:4225-4236 (2001).
Cormier,
R.J., Greenwood, A.C. and Connor, J.A. Bidirectional Synaptic Plasticity
Correlated With the Magnitude of Dendritic Calcium Transients Above a
Threshold.
J.
Neurophysiol. 85: 399-406 (2001).
Connor, J.A. and Cormier, R.J. Cumulative Effects of Glutamate Microstimulation on Ca2+ Responses of CA1 Hippocampal Pyramidal Neurons in Slice. J. Neurophysiol. 83:90-98 (2000).
Connor, J.A., Petrozzino, J.J., Pozzo-Miller, L.D., & Otani, S. Calcium Signals in LTP and LTD, Canadian J. Physiol. & Pharmacol. 77/9:722-734 (1999).
Connor, J.A., Razani-Boroujerdi, S., Greenwood, A.C., Cormier, R.J., Petrozzino, J.J., & Lin, R.C.S. Reduced voltage-dependent Ca2+ signalling in CA1 neurons ater brief ischemia in gerbils. J. Neurophysiol. 81:299-306 (1999)
Otani, S. & Connor, J.A. Requirement of rapid Ca2+ entry and synaptic activation of metabotropic glutamate receptors for the induction of long-term depression in adult rat hippocampus. J. Physiol. (Lond.) 511:761-770 (1998).
Gorter, J.A., Petrozzino, J.J., Aronica, E.M., Rosenbaum, D.M., Opitz, T., Bennett, M.V.L., Connor, J.A., & Zukin R.S. Global ischemia induces downregulation of GluR2 mRNA and increases AMPA receptor-mediated Ca2+ influx in hippocampal CA1 neurons of gerbil. J. Neurosci.17:6179-6188 (1997)
Jonas, E.A., Knox, R.J., Smith, T.C.M., Wayne, N.L., Connor, J.A. & Kaczmarek, L.K. Regulation of a unique neuronal Ca2+ pool and neuropeptide secretion by insulin. Nature 385:343-346 (1997).
Zheng, F., Gallagher, J.P., & Connor, J.A. Activation of a metabotropic excitatory amino acid receptor potentiates spike-driven calcium increases in neurons of the dorsolateral septum.J. Neurosci. 16:6079-6088 (1996).
Yuzaki, M., Forrest, D., Curran, T., & Connor, J.A. Selective activation of calcium permeability by aspartate in Purkinje cells. Science 273:1112-1114 (1996).
Yuzaki, M., Forrest, D., Verselis, L.M., Sun, S.C., Curran, T., & Connor, J.A. Functional NMDA receptors are transiently active and support the survival of Purkinje cells in culture. J. Neurosci. 16:4651-4661 (1996)
McQuiston, A.R., Petrozzino, J.J., Connor, J.A., & Colmers, W.F. Neuropeptide Y1 receptors inhibit N-type calcium currents and reduce transient calcium increases in rat dentate granule cells. J. Neurosci.16:1422-1429 (1996)
Knox, R.J., Jonas, E.A., Kao, L.-S., Smith, P.J.S., Connor, J.A., & Kaczmarek, L.K. Ca2+ influx and activation of a cation current are coupled to intracellular Ca2+ release in peptidergic neurons.J. Physiol. (Lond.) 494.3: 627-639 (1996).
Otani, S. & Connor, J.A. A novel synaptic interaction underlying induction of long-term depression in the area CA1 of adult rat hippocampus. J. Physiol. (Lond.) 492, 225-230 (1996).
Pozzo-Miller, L.D., Petrozzino, J.J., Golari, G.& Connor, J.A. Ca2+ release from intracellular stores induced by afferent stimulation of CA3 pyramidal neurons in hippocampal slices. J. Neurophysiol. 76: 554-562 (1996).
Kasof, G.M., Pozzo-Miller, L.D., Mahanty, N.K., Curran, T., Connor, J.A., & Morgan, J.I. Spontaneous and evoked glutamate signalling influences Fos-lacZ expression and pyramidal cell death in hippocampal slice cultures from transgenic rats. Molecular Brain Research 34: 197-208. (1995).
Pozzo Miller, L.D., Petrozzino, J.J., & Connor, J.A. G protein-coupled receptors mediate a fast excitatory postsynaptic current in hippocampal CA3 pyramidal neurons in brain slice. J. Neurosci. 15: 8320-8330. (1995)
Petrozzino, J.J., Pozzo Miller, L.D., & Connor, J.A. Micromolar Ca2+ transients in dendritic spines of hippocampal pyramidal neurons in brain slice Neuron, 14:1223-1231. (1995).
Otani, S. & Connor, J.A. Long-term depression of naive synapses in adult hippocampus induced by asynchronour synaptic activity. J. Neurophysiol.,. 73:25962601. (1995).
Linden, D.J. & Connor, J.A. Long-term synaptic depression. Ann. Rev. Neurosci., 18:319-357 (1995).
Pozzo Miller, L.D., Mahanty, N.K.,Connor, J.A., & Landis, D.M.D. Spontaneous pyramidal cell death in organotypic slice cultures from rat hippocampus is prevented by glutamate receptor antagonists. Neuroscience, 63:471-487 (1994).
Petrozzino, J.J. & Connor, J.A. Dendritic Ca2+ accumulations and metabotropic glutamate receptor activation associated with an NMDA receptor-independent LTP in hippocampal CA1 neurons. Hippocampus, 4:546-558 (1994)
Forrest, D., Yuzaki, M., Soares, H.D., Ng, L., Luk, D.C., Sheng, M., Stewart, C.L., Morgan, J.I., Connor, J.A., & Curran, T. Targeted disruption of NMDA receptor 1 gene abolishes NMDA response and results in neonatal death. Neuron 13:325-338 (1994).
Yang, X.-D., Connor, J.A., & Faber, D.S. Weak excitation and simultaneous inhibition induce long-term depression in hippocampal CA1 neurons. JNeurophysiol., 71:1586-1590 (1994).
Linden, D.J., Smeyne, M., & Connor, J.A. Trans -ACPD, a metabotropic receptor agonist, produces calcium mobilization and an inward current in cultured cerebellar Purkinje neurons. J. Neurophysiol. 71:1992-1998 (1994).
Zheng, J., Connor, J.A., & Poo, M.M. Turning of nerve growth cones induced by neurotransmitters. Nature 368:140-144 (1994).
Connor, J.A., Pozzo-Miller, L., Petrozzino, J.J., & Muller, W. Calcium signalling in dendritic spines of hippocampal neurons. J. Neurobiology 25:234-242 (1994).
Perkel, D.J., Petrozzino, J.J., Nicoll, R.A., and Connor, J.A. The role of calcium entry via stnaptically-activated NMDA receptors in the induction of long-term potentiation. Neuron 11:817-823 (1993).
Linden, D.L. and Connor, J.A. Induction of cerebellar long-term depression in culture requires postsynaptic action of sodium ions. Neuron 11:193-1100 (1993).
Connor, J.A. Intracellular calcium mobilization by inositol 1,4,5-trisphosphate: intracellular movements and compartmentalization. Cell Calcium 14:185-200 (1993).
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