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Craig Jahr, a senior scientist in the Vollum Institute, holds a concurrent position in the Department of Cell and Developmental Biology in the School of Medicine. After earning his B.A. degree in Psychology from the University of California at Riverside, Jahr studied Biology at the University of California at Santa Barbara. His Ph.D. in Pharmacology was awarded by the University of California at San Francisco in 1980. Jahr did postdoctoral research at UCSF and the Harvard Medical School. He was appointed as an associate research scientist in Molecular Neurobiology at the Yale University School of Medicine in 1985 and remained there until his appointment to the Vollum Institute in 1987. Research InterestsNeurons in the brain transmit information to each other through specialized connections called synapses. Craig Jahr and his coworkers use electrophysiological techniques to focus on synaptic transmission involving the release of glutamate, a chemical neurotransmitter that can cause synaptically connected neurons to become excited. The excitation is generated by the binding of glutamate to specific receptors embedded in the neuronal membrane. Glutamate, like most other neurotransmitters, is released from presynaptic sites following action potential invasion by the fusion of transmitter-filled vesicles to the presynaptic membrane. A widely held belief in neurobiology is that a maximum of a single vesicle can be released per synapse per action potential. Jahr and coworkers have shown that, at a particular type of synapse in the cerebellum, a single action potential can evoke the release of several vesicles per synapse per action potential. This results in a very high concentration of glutamate in the synapse that saturates the postsynaptic receptors and ensures excitation of the postsynaptic neuron. In addition, it appears that vesicular release can occur not only at the presynaptic active zone, but also from other presynaptic locations that are not associated with postsynaptic specializations, including glial membranes. Such ectopic release results in more rapid and complete activation of extrasynaptic receptors and may be necessary to maintain glial membranes close to synapses. Jahr and his colleagues have found that glutamate released from the presynaptic terminal is cleared from the cleft very rapidly, within 2 to 3 milliseconds, despite a lack of an extracellular glutamate-degrading enzyme. Ultimately, released glutamate is taken up into neurons and surrounding astrocytes by glutamate transporters, membrane-spanning proteins that transport extracellular glutamate into cells. Jahr and coworkers have shown that glutamate transporters bind extracellular glutamate very rapidly and then translocate the neurotransmitter into cells, primarily astrocytes. In addition, they have shown that glutamate transporter blockers can prolong the postsynaptic effects of glutamate release, suggesting that glutamate uptake is important for normal synaptic function. Despite this, recent work in the lab suggests that altering the strength of neuronal uptake may determine whether perisynaptically located receptors, such as metabotropic glutamate receptors, are activated by synaptic release. Selected PublicationsMatsui, K. and Jahr, C.E. (2004) Differential control of synaptic and ectopic vesicular release of glutamate. J. Neurosci. 24:8932-8939. Matsui, K. and Jahr, C.E. (2003) Ectopic release of synaptic vesicles. Neuron 40:1173-1183. Harrison, J. and Jahr, C.E. (2003) Receptor occupancy limits synaptic depression at climbing fiber synapses. J. Neurosci. 23:377-383. Delaney, A.J. and Jahr, C.E. (2002) Kainate receptors differentially regulate release at two parallel fiber synapses. Neuron 36:475-482. Bergles, D.E., Tzingounis, A.V., and Jahr, C.E. (2002) Comparison of coupled and uncoupled currents during glutamate uptake by GLT-1 transporters. J. Neurosci. 22:10153-10162. Smith, T.C. and Jahr, C.E. (2002) Self-inhibition of olfactory bulb neurons. Nature Neurosci. 5:760-766. Wadiche, J.I. and Jahr, C.E. (2001) Multivesicular release at climbing fiber-Purkinje cell synapses. Neuron 32:301-313.
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