| The zinc ion has emerged as an important messenger ion in the central nervous system, with evidence suggesting roles in synaptic modulation of amino acid transmission and in excitotoxicity following ischemia, trauma and seizures. The anatomical location and synaptic signaling role of this cation have led to the hypothesis that Zn2+ is released from presynaptic boutons, traverses the synaptic cleft, and enters postsynaptic neurons. However, these events have not been directly observed or characterized.; In the present study, I show vesicular zinc movement in the synapse as “release” and “trans location”. First, I show that electrical stimulation of mossy fibers causes immediate release of Zn 2+ from presynaptic terminals into the extracellular microenvironment using two newly developed fluorescence imaging technique with rat hippocampal slices. The amount of Zn2+ released is dependent on stimulation frequency, action potentials (blocked by TTX) and extracellular Ca 2+. Second, electrical stimulation of Zn2+-containing axons of stratum radiatum of CA1 (Schaffer collaterals) causes Zn2+ translocation into apical dendrite, e.g. (i) the translocation occurs into apical dendrites (where the zinc-containing boutons actually synapse) more vigorously than at the somata, and (ii) there is apparent translocation into dendrites when a zinc-containing synaptic input is stimulated but not when a zinc-free input (direct Temporo Ammonic pathway) to the same dendrite is stimulated. The intradendritic Zn2+ fluorescence rose after stimulation of the Schaffer collaterals was blocked by TTX, Ca 2+ free medium, or the extracellular zinc chelator CaEDTA.; The present study demonstrates that two different zinc movement processes exist, (1) the vesicular zinc release from the presynaptic terminals, (2) the zinc translocation into the postsynaptic apical dendrites after physiological stimulation. |
