We quantified the time delay between the somatic AP burst and the peak of dendritic Ca 2+ transient in the apical tuft, because this delay is important for induction of spike-timing dependent plasticity. In the tuft branches, the density of Na + and K + channels was sufficient to support local initiation of fast spikelets by glutamate iontophoresis. Small perturbations in dendritic physiology, such as spontaneous synaptic inputs, channel inactivation, or temperature-induced changes in channel kinetics, can cause bAP flickering. We found that the amplitude of bAP- Ca 2+ in apical tuft branches was unstable, given that it varied from trial to trial (termed "bAP- Ca 2+ flickering"). To determine whether the efficacy of AP backpropagation into apical tuft dendrites is stable over time, we performed dendritic Ca 2+ and voltage imaging in rat brain slices. In cortical pyramidal neurons, backpropagating action potentials (bAPs) supply Ca 2+ to synaptic contacts on dendrites. Short, Shaina M Oikonomou, Katerina D Zhou, Wen-Liang Acker, Corey D Popovic, Marko A Zecevic, Dejan Antic, Srdjan D The stochastic nature of action potential backpropagation in apical tuft dendrites. The present study provides evidence that synaptically released zinc translocates into postsynaptic neurons through the apical dendrites of CA1 pyramidal neurons during physiological synaptic activity. Genetic depletion of vesicular zinc by ZnT 3 KO showed no stimulation-induced apical dendrite zinc rise. Stimulation of the temporo-ammonic pathway caused no significant rise in the fluorescence. Stimulation of the Schaffer collaterals increased the dendritic fluorescence, which was blocked by TTX, low- Ca medium, or the extracellular zinc chelator, CaEDTA. Burst stimulation (100Hz, 500microA, 0.2ms, monopolar) was delivered to either the adjacent Schaffer-collateral inputs (zinc-containing) or to the adjacent temporo-ammonic inputs (zinc-free) to the CA1 dendrites. After washout, a single apical dendrite in the stratum radiatum of hippocampal CA1 area was selected and focused on. Hippocampal slices were preloaded with the "trappable" zinc fluorescent probe, Newport Green. In the present work I have extended those findings in three ways: (i) providing evidence that zinc translocation occurs into apical dendrites, (ii) presenting data that there is an apparent translocation into apical dendrites when only a zinc-containing synaptic input is stimulated, and (iii) presenting data that there is no zinc translocation into apical dendrite of ZnT 3 KO mice following electrical stimulation. Several studies have previously demonstrated that a brief electrical stimulation is sufficient to induce the translocation of zinc from presynaptic vesicles into the cytoplasm (soma) of postsynaptic neurons. Translocation of the endogenous cation zinc from presynaptic terminals to postsynaptic neurons after brain insult has been implicated as a potential neurotoxic event. Detection of zinc translocation into apical dendrite of CA1 pyramidal neuron after electrical stimulation.
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