Requirement of protein synthesis for group I mGluR-mediated induction of epileptiform discharges

被引:81
作者
Merlin, LR
Bergold, PJ
Wong, RKS
机构
[1] SUNY Hlth Sci Ctr, Dept Neurol, Brooklyn, NY 11203 USA
[2] SUNY Hlth Sci Ctr, Dept Physiol & Pharmacol, Brooklyn, NY 11203 USA
关键词
D O I
10.1152/jn.1998.80.2.989
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Picrotoxin (50 mu M) elicited rhythmic synchronized bursting in CA3 pyramidal cells in guinea pig hippocampal slices. Addition of the selective group I metabotropic glutamate receptor (mGluR) agonist (S)-3,5-dihydroxyphenylglycine (25 mu M) elicited an increase in burst frequency. This was soon followed by a slowly progressive increase in burst duration (BD), converting the brief 250-520 ms picrotoxin-induced synchronized bursts into prolonged discharges of 1-5 s in duration. ED was significantly increased within 60 min and reached a maximum after 2-2.5 h of agonist exposure. The protein synthesis inhibitors anisomycin (15 mu M) or cycloheximide (25 mu M) significantly impeded the mGluR-mediated development of the prolonged bursts; 90-120 min of agonist application failed to elicit the expected burst prolongation. By contrast, the mGluR-mediated enhancement of burst frequency progressed unimpeded. Furthermore, protein synthesis inhibitors had no significant effect on the frequency or duration of fully developed mGluR-induced prolonged discharges. These results suggest that the group I mGluR-mediated prolongation of synchronized bursts has a protein synthesis-dependent mechanism.
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收藏
页码:989 / 993
页数:5
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