Influx of extracellular Zn(2+) into the hippocampal CA1 neurons is required for cognitive performance via long-term potentiation

Physiological significance of synaptic Zn(2+) signaling was examined in the CA1 of young rats. In vivo CA1 long-term potentiation (LTP) was induced using a recording electrode attached to a microdialysis probe and the recording region was locally perfused with artificial cerebrospinal fluid (ACSF) v...

Full description

Saved in:
Bibliographic Details
Published in:Neuroscience 2015-09, Vol.304, p.209-216
Main Authors: Takeda, A, Suzuki, M, Tempaku, M, Ohashi, K, Tamano, H
Format: Article
Language:English
Subjects:
Animals
CA1 Region, Hippocampal - drug effects
CA1 Region, Hippocampal - physiology
Cations - metabolism
Chelating Agents - pharmacology
Chlorides - administration & dosage
Cognition - drug effects
Dose-Response Relationship, Drug
Excitatory Postsynaptic Potentials - drug effects
Extracellular Space - drug effects
Extracellular Space - metabolism
Long-Term Potentiation - drug effects
Male
Memory Disorders - metabolism
Microdialysis
Microelectrodes
Neurons - drug effects
Neurons - physiology
Neuropsychological Tests
Psychotropic Drugs - administration & dosage
Rats, Wistar
Recognition (Psychology) - drug effects
Zinc - metabolism
Zinc Compounds - administration & dosage
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Physiological significance of synaptic Zn(2+) signaling was examined in the CA1 of young rats. In vivo CA1 long-term potentiation (LTP) 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. In vivo CA1 LTP was inhibited under perfusion with CaEDTA and ZnAF-2DA, extracellular and intracellular Zn(2+) chelators, respectively, suggesting that the influx of extracellular Zn(2+) is required for in vivo CA1 LTP induction. The increase in intracellular Zn(2+) was chelated with intracellular ZnAF-2 in the CA1 1h after local injection of ZnAF-2DA into the CA1, suggesting that intracellular Zn(2+) signaling induced during learning is blocked with intracellular ZnAF-2 when the learning was performed 1h after ZnAF-2DA injection. Object recognition was affected when training of object recognition test was performed 1h after ZnAF-2DA injection. These data suggest that intracellular Zn(2+) signaling in the CA1 is required for object recognition memory via LTP. Surprisingly, in vivo CA1 LTP was affected under perfusion with 0.1-1μM ZnCl2, unlike the previous data that in vitro CA1 LTP was enhanced in the presence of 1-5μM ZnCl2. The influx of extracellular Zn(2+) into CA1 pyramidal cells has bidirectional action in CA1 LTP. The present study indicates that the degree of extracellular Zn(2+) influx into CA1 neurons is critical for LTP and cognitive performance.
ISSN:1873-7544
DOI:10.1016/j.neuroscience.2015.07.042