共 59 条
Synaptic Signaling by All-Trans Retinoic Acid in Homeostatic Synaptic Plasticity
被引:304
作者:

Aoto, Jason
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Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

Nam, Christine I.
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Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

Poon, Michael M.
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Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

Ting, Pamela
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Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

Chen, Lu
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Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94720 USA Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
机构:
[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[2] Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94720 USA
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D O I:
10.1016/j.neuron.2008.08.012
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
Normal brain function requires that the overall synaptic activity in neural circuits be kept constant. Longterm alterations of neural activity lead to homeostatic regulation of synaptic strength by a process known as synaptic scaling. The molecular mechanisms underlying synaptic scaling are largely unknown. Here, we report that all-trans retinoic acid (RA), a well-known developmental morphogen, unexpectedly mediates synaptic scaling in response to activity blockade. We show that activity blockade increases RA synthesis in neurons and that acute RA treatment enhances synaptic transmission. The RA-induced increase in synaptic strength is occluded by activity blockade-induced synaptic scaling. Suppression of RA synthesis prevents synaptic scaling. This form of RA signaling operates via a translation-dependent but transcription-independent mechanism, causes an upregulation of postsynaptic glutamate receptor levels, and requires RAR alpha receptors. Together, our data suggest that RA functions in homeostatic plasticity as a signaling molecule that increases synaptic strength by a protein synthesis-dependent mechanism.
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页码:308 / 320
页数:13
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