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Rapid Intracellular Zn2+ Dysregulation via Membrane Corticosteroid Receptor Activation Affects In Vivo CA1 LTP.

Abstract：

:Involvement of membrane mineralocorticoid (MC) and glucocorticoid (GC) receptors in synaptic Zn2+ dynamics remains unclear. Here, we tested whether synaptic plasticity is affected by rapid intracellular Zn2+ dysregulation via membrane MC and GC receptor activation, in comparison with intracellular Ca2+ dysregulation. In anesthetized rats, extracellular Zn2+ level was increased under local perfusion of the hippocampal CA1 with 500 ng/ml corticosterone. In vivo CA1 long-term potentiation (LTP) at Schaffer collateral-CA1 pyramidal cell synapses was attenuated by the pre-perfusion with corticosterone prior to tetanic stimulation, and the attenuation was canceled by co-perfusion with CaEDTA, an extracellular Zn2+ chelator, suggesting that corticosterone-induced increase in extracellular Zn2+ is involved in the subsequent attenuation of LTP. In rat brain slices, corticosterone-induced increases in extracellular and intracellular Zn2+ were blocked in the presence of spironolactone, a MC receptor antagonist that canceled corticosterone-induced attenuation of LTP. Mifepristone, a GC receptor antagonist, which canceled corticosterone-induced attenuation of LTP, also blocked corticosterone-induced increase in intracellular Zn2+, but not extracellular Zn2+. Moreover, corticosterone-induced decrease in phosphorylated CaMKII was restored in the presence of CaEDTA or spironolactone. These results indicate that glucocorticoid rapidly induces the increase in intracellular Zn2+, which occurs via membrane MC and GC receptor activations, and decreases phosphorylated CaMKII level, resulting in attenuating LTP. Membrane MC and GC receptors induce intracellular Zn2+ dysregulation via differential mechanisms. In contrast, glucocorticoid-induced intracellular Ca2+ dysregulation is not crucial for affecting LTP.

journal_name

Mol Neurobiol

journal_title

Molecular neurobiology

authors

Suzuki M,Sato Y,Tamura K,Tamano H,Takeda A

doi

10.1007/s12035-018-1159-9

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

1356-1365

issue

2

eissn

0893-7648

issn

1559-1182

pii

10.1007/s12035-018-1159-9

journal_volume

56

pub_type

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