Stanford Advisors

All Publications

  • A Synaptic Circuit Required for Acquisition but Not Recall of Social Transmission of Food Preference. Neuron Wang, C. Y., Liu, Z. n., Ng, Y. H., Südhof, T. C. 2020


    During social transmission of food preference (STFP), the combination of an olfactory sensory input with a social cue induces long-term memory of a food odor. How a social cue produces long-term learning of an olfactory input, however, remains unknown. Here we show that the neurons of the anterior olfactory nucleus (AON), which form abundant synaptic projections onto granule cells in the olfactory bulb (OB), express the synaptogenic molecule C1ql3. Deletion of C1ql3 in the dorsolateral AON impaired synaptic AON→OB connections and abolished acquisition, but not recall, of STFP memory without significantly affecting basal olfaction. Moreover, deletion in granule cells of the OB of Bai3, a postsynaptic GPCR that binds C1ql3, similarly suppressed synaptic transmission at AON→OB projections and abolished acquisition, but not recall, of STFP memory. Thus, synaptic AON→OB connections are selectively required for STFP memory acquisition and are formed by an essential interaction of presynaptic C1ql3 with postsynaptic Bai3.

    View details for DOI 10.1016/j.neuron.2020.04.004

    View details for PubMedID 32369733

  • How Do Microtubule Dynamics Relate to the Hallmarks of Learning and Memory? JOURNAL OF NEUROSCIENCE Kaganovsky, K., Wang, C. 2016; 36 (22): 5911–13

    View details for PubMedID 27251613

  • Promoting axon regeneration in the adult CNS by modulation of the melanopsin/GPCR signaling. Proceedings of the National Academy of Sciences of the United States of America Li, S. n., Yang, C. n., Zhang, L. n., Gao, X. n., Wang, X. n., Liu, W. n., Wang, Y. n., Jiang, S. n., Wong, Y. H., Zhang, Y. n., Liu, K. n. 2016; 113 (7): 1937–42


    Cell-type-specific G protein-coupled receptor (GPCR) signaling regulates distinct neuronal responses to various stimuli and is essential for axon guidance and targeting during development. However, its function in axonal regeneration in the mature CNS remains elusive. We found that subtypes of intrinsically photosensitive retinal ganglion cells (ipRGCs) in mice maintained high mammalian target of rapamycin (mTOR) levels after axotomy and that the light-sensitive GPCR melanopsin mediated this sustained expression. Melanopsin overexpression in the RGCs stimulated axonal regeneration after optic nerve crush by up-regulating mTOR complex 1 (mTORC1). The extent of the regeneration was comparable to that observed after phosphatase and tensin homolog (Pten) knockdown. Both the axon regeneration and mTOR activity that were enhanced by melanopsin required light stimulation and Gq/11 signaling. Specifically, activating Gq in RGCs elevated mTOR activation and promoted axonal regeneration. Melanopsin overexpression in RGCs enhanced the amplitude and duration of their light response, and silencing them with Kir2.1 significantly suppressed the increased mTOR signaling and axon regeneration that were induced by melanopsin. Thus, our results provide a strategy to promote axon regeneration after CNS injury by modulating neuronal activity through GPCR signaling.

    View details for DOI 10.1073/pnas.1523645113

    View details for PubMedID 26831088

    View details for PubMedCentralID PMC4763730