CA1 LTP Attenuated by Corticosterone is Canceled by Effusol via Rescuing Intracellular Zn 2+ Dysregulation
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ORIGINAL RESEARCH
CA1 LTP Attenuated by Corticosterone is Canceled by Effusol via Rescuing Intracellular Zn2+ Dysregulation Haruna Tamano1 · Yuichi Sato1 · Mako Takiguchi1 · Taku Murakami1 · Toshiyuki Fukuda2 · Hirokazu Kawagishi3 · Miki Suzuki1 · Atsushi Takeda1 Received: 4 February 2019 / Accepted: 27 May 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019
Abstract Exposure to corticosterone attenuates hippocampal CA1 long-term potentiation (LTP) via intracellular Z n2+ dysregulation. Here we report that effusol, a phenanthrene isolated from Chinese medicine Juncus effusus, rescues CA1 LTP attenuated by corticosterone. In vivo microdialysis experiment indicated that both increases in extracellular glutamate induced under perfusion with corticosterone and high K+ are suppressed in the hippocampus by co-perfusion with effusol. Because corticosterone and high K+ also increase extracellular Zn2+ level, followed by intracellular Zn2+ dysregulation, the effect of effusol on both the increases was examined in brain slice experiments. Effusol did not suppress increase in extracellular Z n2+ 2+ in the hippocampal CA1 of brain slices bathed in corticosterone, but suppressed increase in intracellular Zn , which may be linked with suppressing the increase in extracellular glutamate in vivo. In vivo CA1 LTP was attenuated under perfusion with corticosterone prior to LTP induction, while the attenuation was rescued by co-perfusion with effusol, suggesting that the rescuing effect of effusol is due to suppressing the increase in intracellular Zn2+ in CA1 pyramidal cells. The present study indicates that CA1 LTP attenuated by corticosterone is canceled by effusol, which rescues intracellular Zn2+ dysregulation via suppressing extracellular glutamate accumulation. It is likely that effusol defends the hippocampal function against stress-induced cognitive decline. Keywords Effusol · Juncus effusus · Zn2+ · Corticosterone · Hippocampus · Stress Abbreviations LTP Long-term potentiation MC Mineralocorticoid GC Glucocorticoid CS Corticosterone AMPA α-Amino-3-hydroxy-5-methyl-4isoxazolepropionate GABA γ-Aminobutyric acid ACSF Artificial cerebrospinal fluid
* Atsushi Takeda takedaa@u‑shizuoka‑ken.ac.jp 1
Department of Neurophysiology, School of Pharmaceutical Sciences, University of Shizuoka, 52‑1 Yada, Suruga‑ku, Shizuoka 422‑8526, Japan
2
Satoen CO., LTD, 1057 Ohhara, Aoi‑ku, Shizuoka 421‑1392, Japan
3
Research Institute of Green Science and Technology, Shizuoka University, 836 Ohya, Suruga‑ku, Shizuoka 422‑8529, Japan
PCL Pyramidal cell layer SR Stratum radiatum
Introduction Exposure to stress activates the hypothalamo-pituitaryadrenocortical axis, followed by increasing glucocorticoid (GC) secretion from the adrenal cortex. When blood glucocorticoid concentration is increased, glucocorticoid transport to the brain extracellular fluid is increased through the blood–brain barrier. This increase modifies cognitive activity bidirectionally (McEwen and Sapolsky 1995; Kim and
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