ERK plays a regulatory role in induction of LTP by theta frequency stimulation and its modulation by β-adrenergic receptors

被引:286
作者
Winder, DG
Martin, KC
Muzzio, IA
Rohrer, D
Chruscinski, A
Kobilka, B
Kandel, ER
机构
[1] Columbia Univ Coll Phys & Surg, Ctr Neurobiol & Behav, New York State Psychiat Inst, Howard Hughes Med Inst, New York, NY 10032 USA
[2] Stanford Univ, Howard Hughes Med Inst, Dept Med, Stanford, CA 94305 USA
关键词
D O I
10.1016/S0896-6273(00)81124-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
MAP kinase (ERK) translates cell surface signals into alterations in transcription. We have found that ERK also regulates hippocampal neuronal excitability during 5 Hz stimulation and thereby regulates forms of long-term potentiation (LTP) that do not require macromolecular synthesis. Moreover, ERK-mediated changes in excitability are selectively required for some forms of LTP but not others. ERK is required for the early phase of LTP elicited by brief 5 Hz stimulation, as well as for LTP elicited by more prolonged 5 Hz stimulation when paired with beta 1-adrenergic receptor activation. By contrast, ERK plays no role in LTP elicited by a single 1 s 100 Hz train. Consistent with these results, we find that ERK is activated by beta-adrenergic receptors in CA1 pyramidal cell somas and dendrites.
引用
收藏
页码:715 / 726
页数:12
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