Involvement of intracellular Zn2+ signaling in LTP at perforant pathway –CA1 pyramidal cell synapse

Abstract
Physiological significance of synaptic Zn2+ signaling was examined at perforant pathway–CA1 pyramidal cell synapses. In vivo long‐term potentiation (LTP) at perforant pathway–CA1 pyramidal cell synapses was induced using a recording electrode attached to a microdialysis probe and the recording region was locally perfused with artificial cerebrospinal fluid (ACSF) via the microdialysis probe. Perforant pathway LTP was not attenuated under perfusion with CaEDTA (10 mM), an extracellular Zn2+ chelator, but attenuated under perfusion with ZnAF‐2DA (50 μM), an intracellular Zn2+ chelator, suggesting that intracellular Zn2+ signaling is required for perforant pathway LTP. Even in rat brain slices bathed in CaEDTA in ACSF, intracellular Zn2+ level, which was measured with intracellular ZnAF‐2, was increased in the stratum lacunosum‐moleculare where perforant pathway–CA1 pyramidal cell synapses were contained after tetanic stimulation. These results suggest that intracellular Zn2+ signaling, which originates in internal stores/proteins, is involved in LTP at perforant pathway–CA1 pyramidal cell synapses. Because the influx of extracellular Zn2+, which originates in presynaptic Zn2+ release, is involved in LTP at Schaffer collateral‐CA1 pyramidal cell synapses, synapse‐dependent Zn2+ dynamics may be involved in plasticity of postsynaptic CA1 pyramidal cells.

Source: Hippocampus - April 13, 2017 Category: Neurology Authors: Haruna Tamano, Ryusuke Nishio, Atsushi Takeda Tags: RESEARCH ARTICLE Source Type: research