Zinc released from glutamatergic vesicle in the hippocampus, auditory cortex, olfactory bulb, and optic nerve has both physiological and pathological consequences. Through the use of chelating agents that rapidly sequester this mobilized zinc, and by the application of fluorescent sensors to detect the time- and position-sensitive movement of the ion, we have recorded (i) single synapse release of vesicular zinc in the hippocampus; (ii) modulation of extrasynaptic NMDA receptors by synaptic and tonic zinc in cartwheel cells, a class of inhibitory interneurons in the molecular layer of the dorsal cochlear nucleus that receive glutamatergic input from synaptic zinc-rich parallel fibers; (iii) release of zinc from glomeruli in the olfactory bulb upon electrophysiological stimulation in slices and as delineated in sensory maps produced in live animals following exposure to specific odorants; and (iv) mobile zinc release in the inner plexiform layer of the retina following optic nerve crush, a phenomenon used to guide the application of a fast zinc chelator as a means to promote optic nerve regeneration following crush. This work was supported by a grant from the National Institute of General Medical Sciences.

Mobile zinc signaling in the brain – learning, memory, hearing, olfaction, and vision

249th National Meeting (2015)

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