ApTrkl, a Trk-like receptor, mediates serotonin-dependent ERK activation and long-term facilitation in Aplysia sensory neurons

被引：45

作者：

Ormond, J

Hislop, J

Zhao, YL

Webb, N

Vaillaincourt, F

Dyer, JR

Ferraro, G

Barker, P

Martin, KC

Sossin, WS

机构：

[1] McGill Univ, Montreal Neurol Inst, Montreal, PQ H3A 2B4, Canada

[2] Univ Calif Los Angeles, Dept Psychiat Biobehav Sci, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA

[4] Univ Calif Los Angeles, Dept Biol Chem, Los Angeles, CA 90095 USA

来源：

NEURON | 2004年 / 44卷 / 04期

基金：

加拿大健康研究院;

关键词：

D O I：

10.1016/j.neuron.2004.11.001

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The Trk family of receptor tyrosine kinases plays a role in synaptic plasticity and in behavioral memory in mammals. Here, we report the discovery of a Trk-like receptor, ApTrkl, in Aplysia. We show that it is expressed in the sensory neurons, the locus for synaptic facilitation, which is a cellular model for memory formation. Serotonin, the facilitatory neurotransmitter, activates ApTrkl, which, in turn, leads to activation of ERK. Finally, inhibiting the activation of ApTrkl with the Trk inhibitor K252a or using dsRNA to inhibit ApTrkl blocks the serotonin-mediated activation of ERK in the cell body, as well as the cell-wide long-term facilitation induced by 5-HT application to the cell body. Thus, transactivation of the receptor tyrosine kinase ApTrkl by serotonin is an essential step in the biochemical events leading to long-term facilitation in Aplysia.

引用

收藏

页码：715 / 728

页数：14

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