
Liqun Luo
VerifiedStanford University · Biology
Active 1992–2026
About
Liqun Luo is the Ann and Bill Swindells Professor in the School of Humanities and Sciences, Professor of Biology, and Professor of Neurobiology by courtesy at Stanford University. He earned his bachelor's degree in molecular biology from the University of Science and Technology of China in 1986 and completed his Ph.D. in Biology at Brandeis University in 1992. Following postdoctoral training at the University of California, San Francisco, he started his own lab in the Department of Biology at Stanford University in December 1996. Dr. Luo's research focuses on how neural circuits are assembled during development and how their architectures enable specific functions in adults. He studies the genetic analysis of neural circuit organization and assembly in flies and mice. As a Howard Hughes Medical Institute Investigator, he has contributed significantly to the understanding of neural circuit development. Dr. Luo is also the author of the widely used textbook 'Principles of Neurobiology,' now in its second edition. He has served on the editorial boards of several prominent scientific journals and has received numerous awards, including the McKnight Technological Innovation in Neuroscience Award, the Society for Neuroscience Young Investigator Award, and the Jacob Javits Award from the National Institute of Neurological Disorders and Stroke. He is a member of the National Academy of Sciences and a Fellow of the American Academy of Arts and Sciences.
Research topics
- Biology
- Computer Science
- Genetics
- Neuroscience
- Data Mining
- Artificial Intelligence
- Database
- Cell biology
- Endocrinology
- Computational biology
- Immunology
- Anatomy
- Psychology
- Evolutionary biology
- Medicine
- Chemistry
- Operating system
Selected publications
Stanford Digital Repository · 2026-04-10
datasetOpen accessSenior authorSupplementary Data 1. Interactive visualization of Ten3 and Lphn2 expression in horizonal sections of E17 and P2 mouse brains, related to Figure 1 To visualize the datasets, download all files from (Supplemental Data 1). To visualize E17 data, open the file Ten3_Lphn2_E17.tif in Fiji by dragging it into the Fiji console. Next, launch the ROI manager in Fiji (Analyze > Tools > ROI Manager) and load the file E17_ROIs.zip. Each ROI corresponds to a defined region of interest: clicking on the ROI names will allow you to view Ten3 and Lphn2 expression across respective regions. Same for P2. Ten3 is in cyan and Lphn2 is in yellow.
Stanford Digital Repository · 2026-04-30
articleOpen accessOpioids are widely prescribed to relieve pain, but have high addictive potential due in part to their ability to increase dopamine release in mesolimbic reward circuits. Serotonin signaling is thought to modulate opioid signaling and dopamine release and may mitigate the addictive properties of opioids, including risk of relapse and withdrawal. However, the mechanisms behind this interaction are poorly understood. Preliminary data from our research group suggests that global serotonin release caused by the serotonin-releasing drug (-)-fenfluramine can block opioid-driven addictive behaviors while paradoxically potentiating dopamine release. This finding challenges the prevailing assumption that dopamine release is sufficient to drive addictive behavior and suggests a role for specific serotonin (5-HT) receptor subtypes in decoupling dopamine release from drug reward. Using in vivo fluorescent dopamine reporters and conditioned place preference (CPP) behavioral assays in mice, this study evaluates the effect of specific 5-HT receptor subtype signaling (5-HT1A, 5-HT2A, and 5-HT2B) on opioid-induced dopamine release in the nucleus accumbens (NAc) and addictive behavior. We found that activation of the 5-HT1A receptor increases morphine-induced dopamine release, however it did not block morphine-induced place preference. These results provide insight into how serotonin signaling can be used to modulate the neurobiological pathways of opioid addiction and indicate that targeting the 5-HT1A receptor may not have therapeutic potential in treating opioid addiction.
Current Biology · 2025-08-15 · 2 citations
preprintOpen accessSenior authorCorrespondingEndosome-associated Rab GTPases control distinct aspects of neural circuit assembly
eLife · 2025-11-20
articleOpen accessNeural circuit assembly relies on the precise regulation of cell-surface receptors that mediate signaling and adhesion. Endocytosis controls receptor activity and availability by internalizing and routing proteins through two main pathways: recycling back to the cell-surface or delivery to lysosomes for degradation. Rab GTPases direct receptors into these distinct pathways, but their specific contributions to circuit formation remain opaque. Using clonal analyses with null alleles, we dissected the roles of Rab-mediated trafficking to early, late, and recycling endosomes across multiple stages of circuit assembly in vivo. Our approach revealed that Rab5 and Rab11 regulated extensive and largely distinct developmental events, highlighting the pivotal roles of early endosome sorting and recycling pathways in circuit assembly. We found that as neurons mature, both the spatial distribution and abundance of specific endocytic compartments change to reflect evolving trafficking demands. Our findings underscore how distinct post-endocytic trafficking fates are necessary to build neural circuits.
A molecular basis of somatotopic map formation
bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-15 · 1 citations
preprintOpen accessSomatotopy is a recurring organisational feature of the somatosensory system where adjacent neurons and their connections represent adjacent regions of the body. The molecular mechanisms governing the formation of such "body maps" remain largely unknown. Here we demonstrate that the cell surface proteins teneurin-3 and latrophilin-2 are expressed in opposing gradients in multiple somatotopic maps in the mouse, including within the dorsal horn of the spinal cord. Genetic manipulation of these proteins in spinal dorsal horn or sensory neurons distorts the somatotopy of neuronal connections and impairs accurate localisation of a noxious stimulus on the surface of the body. Our work provides the foundation for a molecular model of somatotopic map formation and insights into their function in the localisation of somatosensory stimuli or topognosis.
Rewiring an olfactory circuit by altering cell-surface combinatorial code
Nature · 2025-11-19 · 4 citations
articleOpen accessSenior authorAbstract Proper brain function requires the precise assembly of neural circuits during development. Despite the identification of many cell-surface proteins (CSPs) that help guide axons to their targets 1,2 , it remains mostly unknown how multiple CSPs work together to assemble a functional circuit. Here we used synaptic partner matching in the Drosophila olfactory circuit 3,4 to address this question. By systematically altering the combination of differentially expressed CSPs in a single type of olfactory receptor neuron (ORN), which senses a male pheromone that inhibits male–male courtship, we switched its connection nearly completely from its endogenous postsynaptic projection neuron (PN) type to a new PN type that promotes courtship. From this switch, we deduced a combinatorial code including CSPs that mediate both attraction between synaptic partners and repulsion between non-partners 5,6 . The anatomical switch changed the odour response of the new PN partner and markedly increased male–male courtship. We generalized three manipulation strategies from this rewiring—increasing repulsion with the old partner, decreasing repulsion with the new partner and matching attraction with the new partner—to successfully rewire a second ORN type to multiple distinct PN types. This work shows that manipulating a small set of CSPs is sufficient to respecify synaptic connections, paving the way to investigations of how neural systems evolve through changes of circuit connectivity.
Endocytome profiling uncovers cell-surface protein dynamics underlying neuronal connectivity
bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-29 · 2 citations
preprintOpen accessSenior authorCorrespondingEndocytosis actively remodels the neuronal surface proteome to drive diverse cellular processes, yet its global extent and circuit-level consequences have defied comprehensive interrogation. Here, we introduce endocytome profiling: a systematic, cell-type-specific approach for mapping cell-surface protein (CSP) dynamics in situ. Quantitative proteomic analysis of developing olfactory receptor neuron (ORN) axons generated an endocytic atlas comprising over 1,100 proteins and revealed the extent to which the surface proteome is remodeled to meet distinct developmental demands. Targeted interrogation of a junctional CSP showed that its endosome-to-surface ratio is precisely balanced to enable developmental axon pruning while preserving mature axon integrity. Multi-omic integration uncovered wide-spread transcellular signaling and identified a growth factor secreted by neighboring neurons to direct ORN axon targeting via endocytic regulation of its receptor. Endocytome profiling thus provides unprecedented access to cell-surface proteome dynamics and offers a powerful platform for dissecting proteome remodeling across diverse cell types and contexts.
Dimensionality reduction simplifies synaptic partner matching in an olfactory circuit
Science · 2025-05-01 · 12 citations
articleOpen accessSenior authorCorrespondingA navigating axon faces complex choices when selecting postsynaptic partners in a three-dimensional (3D) space. In this work, we discovered a principle that can establish the 3D glomerular map of the fly antennal lobe by reducing the higher dimensionality serially to 1D projections. During development, olfactory receptor neuron (ORN) axons first contact their partner projection neuron dendrites on the spherical surface of the antennal lobe, regardless of whether the adult glomeruli lie near the surface or inside. Along this 2D surface, axons of each ORN type take a specific, arc-shaped trajectory that precisely intersects with their partner dendrites. Altering axon trajectories compromises synaptic partner matching. A 3D search is thus reduced to one dimension, simplifying partner matching.
Endosome-associated Rab GTPases control distinct aspects of neural circuit assembly
bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-10
preprintOpen accessNeural circuit assembly relies on the precise regulation of cell-surface receptors that mediate signaling and adhesion. Endocytosis controls receptor activity and availability by internalizing and routing proteins through two main pathways: recycling back to the cell-surface or delivery to lysosomes for degradation. Rab GTPases direct receptors into these distinct pathways, but their specific contributions to circuit formation remain opaque. Using clonal analyses with null alleles, we dissected the roles of Rab-mediated trafficking to early, late, and recycling endosomes across multiple stages of circuit assembly in vivo . Our approach revealed that Rab5 and Rab11 regulated extensive and largely distinct developmental events, highlighting the pivotal roles of early endosome sorting and recycling pathways in circuit assembly. We found that as neurons mature, both the spatial distribution and abundance of specific endocytic compartments change to reflect evolving trafficking demands. Our findings underscore how distinct post-endocytic trafficking fates are necessary to build neural circuits.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-09
articleOpen accessAbstract/Summary The development of β-amyloid (Aβ) pathology in Alzheimer’s disease (AD) is accompanied by profound changes in astrocytes and microglia. How these responses are orchestrated by cell surface proteins, key mediators of cell-cell communication, remain unclear. Using in situ astrocyte cell-surface proteome profiling in 5xFAD mice, we identified a set of dysregulated surface proteins induced by Aβ pathology, including CD44. CD44 was selectively upregulated in plaque-adjacent astrocytes and interacted with osteopontin (OPN), encoded by the disease-associated microglia gene Spp1 , to promote lipid accumulation, and this effect is γ-secretase dependent. Astrocytic CD44 in turn regulated Spp1 expression and microglial activity. Conditional deletion of Cd44 in adult astrocytes of 5xFAD mice attenuated glial reactivity, reduced Aβ pathology, and improved cognition. These findings define a plaque-proximal OPN–CD44 axis that controls astrocyte lipid metabolism and glial activity, positioning CD44 as a surface-accessible therapeutic target in AD.
Recent grants
Cell-cell communications in neural circuit assembly
NIH · $7.3M · 2005–2026
NIH · $1.2M · 2005
NIH · $2.6M · 2013
BRAIN EAGER: Genetic Access of Neuronal Populations Activated by Two Experiences in the Same Animal
NSF · $300k · 2016–2017
Assembly of the Central Olfactory Networks in Drosophila
NIH · $8.1M · 2003–2028
Frequent coauthors
- 150 shared
Stephen R. Quake
Stanford University
- 140 shared
David J. Luginbuhl
Stanford University
- 140 shared
Hongjie Li
Baylor College of Medicine
- 113 shared
Jun Li
Janelia Research Campus
- 109 shared
Qijing Xie
Howard Hughes Medical Institute
- 108 shared
Tongchao Li
Stanford University
- 74 shared
Chuanyun Xu
Howard Hughes Medical Institute
- 72 shared
Mark J. Wagner
Labs
Luo LabPI
Education
- 1992
PhD, Biology
Brandeis University
- 1986
BS, Biology
University of Science and Technology of China
Awards & honors
- McKnight Technological Innovation in Neuroscience Award
- Society for Neuroscience Young Investigator Award
- Jacob Javits Award from National Institute of Neurological D…
- HW Mossman Award from American Association of Anatomists
- Lawrence Katz Prize
- Resume-aware match score
- Save to shortlist
- AI-drafted outreach
See your match with Liqun Luo
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
- Free to start
- No credit card
- 30-second signup