Excess influx of Zn(2+) into dentate granule cells affects object recognition memory via attenuated LTP
Abstract
The influx of extracellular Zn(2+) into dentate granule cells is nonessential for dentate gyrus long-term potentiation (LTP) and the physiological significance of extracellular Zn(2+) dynamics is unknown in the dentate gyrus. Excess increase in extracellular Zn(2+) in the hippocampal CA1, which is induced with excitation of zincergic neurons, induces memory deficit via excess influx of Zn(2+) into CA1 pyramidal cells. In the present study, it was examined whether extracellular Zn(2+) induces object recognition memory deficit via excess influx of Zn(2+) into dentate granule cells. KCl (100 mM, 2 µl) was locally injected into the dentate gyrus. The increase in intracellular Zn(2+) in dentate granule cells induced with high K(+) was blocked by co-injection of CaEDTA and CNQX, an extracellular Zn(2+) chelator and an AMPA receptor antagonist, respectively, suggesting that high K(+) increases the influx of Zn(2+) into dentate granule cells via AMPA receptor activation. Dentate gyrus LTP induction was attenuated 1 h after KCl injection into the dentate gyrus and also attenuated when KCl was injected 5 min after the induction. Memory deficit was induced when training of object recognition test was performed 1 h after KCl injection into the dentate gyrus and also induced when KCl was injected 5 min after the training. High K(+)-induced impairments of LTP and memory were rescued by co-injection of CaEDTA. These results indicate that excess influx of Zn(2+) into dentate granule cells via AMPA receptor activation affects object recognition memory via attenuated LTP induction. Even in the dentate gyrus where is scarcely innervated by zincergic neurons, it is likely that extracellular Zn(2+) homeostasis is strictly regulated for cognition.
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The hippocampal dentate gyrus is involved in NOP processing as evidenced by destruction of high K+ infusions into the region leading to NOP deficits, either treated before or after the sample trial.
“The hippocampal dentate gyrus is involved in NOP processing as evidenced by destruction of high K+ infusions into the region leading to NOP deficits, either treated before or after the sample trial (Suzuki et al., 2015).”
From The medial prefrontal cortex - hippocampus circuit that integrates information of object, place and time to construct episodic memory in rodents: Behavioral, anatomical and neurochemical properties (2020) · cites this paper as Suzuki et al., 2015
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- Authors
- Suzuki, M., Fujise, Y., Tsuchiya, Y., Tamano, H., & Takeda, A.
- Affiliations
- Shizuoka University (JP)
- Corresponding author
- Takeda, Atsushi
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 87
- Pages
- 60-65
- ISSN
- 0197-0186 (ISSN-L)
- OpenAlex
- W624209810
- Cited by
- 34
- References
- 35
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 6 · 2017: 9 · 2016: 4 · 2015: 3
- FWCI
- 4.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurochemistry International (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (25293032)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- extracellular zinc, dentate gyrus, dentate gyrus granule cells, long-term potentiation, object recognition memory, zinc influx, AMPA receptors, high potassium, zinc chelation, CaEDTA, CNQX, zinc homeostasis, hippocampus, memory impairment
- MeSH terms
- Animals, Learning, Male, Memory, Potassium, Zinc, Long-Term Potentiation, Dentate Gyrus, Rats
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