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B.Sc., Ph.D. (Southampton)

  • Professor
  • Physiology
  • The general theme of my research is the physiological and pathophysiological role of calcium in the central nervous system. Central to these studies are the actions of neuron specific calcium-binding proteins in the regulation of intracellular calcium ion concentration and in mediating the actions of calcium as a second messenger system. I have mostly been involved with work investigating calbindin D-28k, (formerly known as calcium-binding protein; CaBP) and parvalbumin (PV). Both proteins were originally discovered in peripheral tissues (gut and muscle, respectively), but are also found in discrete neuronal populations within the CNS. Since these proteins have not been shown to have modulatory actions similar to calmodulin they are thought to act as intracellular calcium buffering proteins.

    I have attempted to apply a multidisciplinary approach to my studies and have thus utilized biochemical, immunohistochemical, electro-physiological, molecular biological and neuroanatomical techniques. The following represents an outline of the major projects currently underway in my laboratory:

    • CaBP and PV: changes in animal models of epilepsy including kindling.
    • CaBP and PV related to neuron death induced by ischemia.
    • CaBP and its calcium buffering effects on glutamate induced calcium influx, determined by calcium imaging techniques in cultured neurons.
    • Anatomical studies of neuron specific projections to the rat hippocampal formation.
    • CaBP and PV localization in human brain material derived from a variety of diseases with established patterns neuronal degeneration.
    • Studies of calcium buffering mechanisms and the effect of artificial calcium buffers in cultured hippocampal neurons related to neuron death induced by excitotoxicity.

    Additional information can be found at the Baimbridge Lab Website.

    Burke RE, Baimbridge KG (1993). Relative loss of striatal striosome compartment, defined by calbindin-D28k immunostaining, following developmental hypoxic-ischemic injury. J Neurosci 56:305-315.

    Yamada T, McGeer PL, Baimbridge KG, McGeer EG (1990). Relative sparing in Parkinson's disease of substantia nigra dopamine neurons containing calbindin D28k. Brain Res 526:303-307.

    Baimbridge KG, Peet MJ, McLennan H, Church J (1991). Bursting response to current-evoked depolarization in rat CA1 pyramidal neurons is correlated to Lucifer Yellow dye coupling but not to the presence of Calbindin D-28k. Synapse 7:269-277.

    Mudrick LA, Baimbridge KG (1991). Hippocampal neurons transplanted into ischemically lesioned hippocampus: Anatomical assessment of survival, maturation and integration. Exptl Brain Res 86:233-247.

    Baimbridge KG, Celio MR, Rogers JH (1992). Calcium-binding proteins in the nervous system. TINS 15:303-308.



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