| Autor: |
Trinh MA; Center for Neural Science, New York University, New York, New York 10003, USA., Ma T, Kaphzan H, Bhattacharya A, Antion MD, Cavener DR, Hoeffer CA, Klann E |
| Jazyk: |
angličtina |
| Zdroj: |
Learning & memory (Cold Spring Harbor, N.Y.) [Learn Mem] 2014 Apr 16; Vol. 21 (5), pp. 298-304. Date of Electronic Publication: 2014 Apr 16. |
| DOI: |
10.1101/lm.032219.113 |
| Abstrakt: |
The proper regulation of translation is required for the expression of long-lasting synaptic plasticity. A major site of translational control involves the phosphorylation of eukaryotic initiation factor 2 α (eIF2α) by PKR-like endoplasmic reticulum (ER) kinase (PERK). To determine the role of PERK in hippocampal synaptic plasticity, we used the Cre-lox expression system to selectively disrupt PERK expression in the adult mouse forebrain. Here, we demonstrate that in hippocampal area CA1, metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) is associated with increased eIF2α phosphorylation, whereas stimulation of early- and late-phase long-term potentiation (E-LTP and L-LTP, respectively) is associated with decreased eIF2α phosphorylation. Interesting, although PERK-deficient mice exhibit exaggerated mGluR-LTD, both E-LTP and L-LTP remained intact. We also found that mGluR-LTD is associated with a PERK-dependent increase in eIF2α phosphorylation. Our findings are consistent with the notion that eIF2α phosphorylation is a key site for the bidirectional control of persistent forms of synaptic LTP and LTD and suggest a distinct role for PERK in mGluR-LTD. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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