Synaptic signaling by all-trans retinoic acid in homeostatic synaptic plasticity

By Jason Aoto, Christine I. Nam, M. M. Poon, P. Ting, Lu Chen. 2008

373 citations recorded by the source corpus.

SUMMARY Normal brain function requires that the overall synaptic activity in neural circuits be kept constant. Long-term alterations of neural activity leads 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 novel form of RA signaling operates via a translation-dependent but transcription-independent mechanism, causes an up-regulation of postsynaptic glutamate receptor levels, and requires RARα 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.

Subfields: Cellular and Molecular Neuroscience, Materials Chemistry, Molecular Biology

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

  1. Friedemann Zenke
  2. Surya Ganguli
  3. Wulfram Gerstner
  4. Gina G. Turrigiano
  5. Pierre Yger
  6. Niraj S. Desai
  7. Matthieu Gilson
  8. D. Feldman

In Molecular Biology

  1. Wulfram Gerstner
  2. Friedemann Zenke
  3. Surya Ganguli
  4. Gina G. Turrigiano
  5. Pierre Yger

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