About

Minghong Ma, Ph.D., is a Professor of Neuroscience at the University of Pennsylvania's Perelman School of Medicine. His research focuses on how the brain perceives and responds to sensory stimuli in both health and disease, utilizing studies with animal models, primarily mice, and human tissues. His work investigates the olfactory system, which is crucial for behaviors such as locating food, communication, and danger avoidance, and explores how olfactory sensory neurons transmit information to the brain, functioning also as mechanosensors conveying nasal breathing signals. Dr. Ma's research emphasizes the network connections between the olfactory system and non-olfactory brain regions, the interaction between respiration and behavioral or mental states, the role of sniffing in neural representation of sensory salience, neural mechanisms underlying interbrain synchrony in socially engaged mice, and the effects of drugs on human neocortical and hippocampal neurons. His laboratory employs techniques such as electrophysiology, neural circuit tracing, optogenetics, chemogenetics, and machine learning. He has contributed extensively to understanding the neural mechanisms of olfactory processing and its implications for neuropsychiatric disorders.

Research topics

• Neuroscience
• Biology
• Psychology
• Chemistry
• Cell biology

Selected publications

• An oxytocin-gated circuit from the hypothalamus silences olfactory tubercle neurons to drive prosocial grooming

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-28

  articleOpen access

  Abstract Spontaneous helping behaviors such as allogrooming are vital for survival in social species, yet their underlying neural mechanisms remain largely unknown. Although oxytocin (OXT) is known to modulate allogrooming, the precise neural circuits, molecular pathways, and sensory drivers remain unclear. Here, using a social emergency paradigm in mice, we show that observer mice selectively allogroom distressed, anesthetized conspecifics, a behavior that is guided by main olfactory system cues and mitigates the demonstrator’s anxiety. We identify an oxytocinergic circuit from the paraventricular hypothalamus to the medial olfactory tubercle (PVN OXT →mOT) that is necessary and sufficient for this helping behavior. In vivo fiber photometry reveals that PVN OXT →mOT activity and OXT release are temporally locked to allogrooming initiation. This behavioral effect requires oxytocin receptor (OXTR) signaling specifically on mOT dopamine D1 receptor-expressing neurons, where OXTRs suppress neuronal excitability via G protein-gated inwardly rectifying K + (GIRK) channels. Disruption of this inhibitory mechanism induces neuronal hyperexcitability and impairs allogrooming, a deficit rescued by restoring GIRK function. These findings define a PVN OXT -mOT circuit for prosocial helping, revealing an oxytocinergic pathway with potential therapeutic relevance for neuropsychiatric disorders characterized by social deficits.

  PublisherOA PDFDOI

• A novel iPSC model of Bryant-Li-Bhoj neurodevelopmental/neurodegenerative syndrome demonstrates the role of histone H3.3 in chromatin dynamics, neuronal differentiation, and maturation

  Journal of Translational Medicine · 2026-02-13

  articleOpen access

  BACKGROUND: Bryant-Li-Bhoj neurodevelopmental syndrome (BLBS) is neurogenetic disorder caused by variants in H3-3A and H3-3B, the two genes that encode histone H3.3. Ninety-nine percent of individuals with BLBS show developmental delay/intellectual disability, but the mechanism by which variants in H3.3 result in these phenotypes is not yet understood, limiting the therapeutic interventions available to individuals living with BLBS. METHODS: Here, we investigate how one BLBS-causative variant, H3-3B p.Leu48Arg (L48R), affects neurodevelopment using an induced pluripotent stem cell model differentiated to 2D neural progenitor cells (NPCs), 2D forebrain neurons (FBNs), and 3D dorsal forebrain organoids (DFBOs). We employ a multi-omic approach in the 2D models to quantify the resulting changes in gene expression and chromatin accessibility. We used immunofluorescence (IF) staining to define the identities of cells in the 3D DFBOs and whole-cell patch clamp to investigate the electrophysiological properties of neurons in DFBOs. RESULTS: In the 2D systems, we found dysregulated gene expression and chromatin accessibility affecting neuronal fate, adhesion, neurotransmission, and excitatory/inhibitory balance. Immunofluorescence of DFBOs corroborated altered proportions of radial glia and mature neuronal populations. Patch clamp recordings revealed decreased electrical activity in neurons from L48R DFBOs compared to control DFBOs. CONCLUSIONS: These data provide the first mechanistic insights into the pathogenesis of BLBS from a human-derived model of neurodevelopment, which suggest that H3.3 L48R increases H3-3B expression, resulting in the hyper-deposition of H3.3 into the nucleosome, which underlies changes in gene expression and chromatin accessibility. Functionally, this causes dysregulation of cell adhesion, neurotransmission, and the balance between excitatory and inhibitory signaling. These results are a crucial step towards preclinical development and testing of targeted therapies for this and related disorders.

  PublisherDOI

• Author Correction: Leveraging deep single-soma RNA sequencing to explore the neural basis of human somatosensation

  Nature Neuroscience · 2026-03-06

  articleOpen access

  In the version of this article initially published, several figure elements were incorrect.In Fig. 4c, the labels "hPEP.PIEZo h ", "hAb.LTMR", and "hAd.LTMR" should have read "hPEP.PIEZO h ", "hA.LTMR", and "hA.LTMR", respectively.In Fig. 4d, the positions of the x-axis labels "CHRNA7" and "KIT" were swapped.In Fig. 4e, the panels for "hPEP.NTRK3" and "hA.LTMR" inadvertently showed the same image; the "hA.LTMR" panel has been replaced with the correct image.In Fig. 8i, the label "C-HTMR Heat + " should be "C-HTMR Cool + ."Also, in Fig. 8i, the axis tick label "20" was a typographical concatenation and should appear as two separate ticks, "2" and "0."In Fig. 8i-j, the label "noxious range" has been removed; the grey shading is intended only to indicate the sustained phase (already denoted by "0 C sustained" and "50 C sustained").These errors have

  PublisherOA PDFDOI

• A midbrain-to-ventral-striatum dopaminergic pathway orchestrates odor-guided insect predation in mice

  Proceedings of the National Academy of Sciences · 2025-10-10 · 2 citations

  articleOpen accessCorresponding

  Foraging and food consumption are fundamental for the survival of animals. In natural environments, wild rodents feed on insects, including moth larvae, and odor-guided evaluation of potential food resources is a critical step in initiating feeding behavior. However, the mechanisms by which rodents seek and feed on insect prey remain poorly understood. Herein, we employed a laboratory-based predator-prey interaction system using mice and cotton bollworm larvae to investigate the neural mechanisms underlying food-seeking and feeding behaviors at both cellular and neural circuit levels. We demonstrate that mice exhibit a strong preference for consuming fed larvae, and this preference is dependent on the main olfactory system. Gas chromatography-mass spectrometry analysis revealed significant differences in the chemical profiles of fed and unfed larvae, with fed larvae containing a higher level of linoleic acid (LA) and a lower level of (Z)-9-tricosene [(Z)-9-TE]. Behavioral assays showed that mice, as well as Brand's voles and brown rats, are attracted to LA but avoid (Z)-9-TE in a two-choice odor preference test. Furthermore, we identified that the dopaminergic pathway from the ventral tegmental area (VTA) to the medial olfactory tubercle (mOT) plays a central role in mediating this preference. Chemogenetic inhibition of this pathway abolished the preference for LA over (Z)-9-TE, while chemogenetic activation reversed this effect. Additionally, fiber photometry recordings and pharmacology revealed that mOT D1 and D2 spiny projection neurons preferentially mediate attraction to LA and avoidance of (Z)-9-TE, respectively. These findings uncover a neurobiological system in rodents that supports insect predation based upon chemosignals.

  PublisherDOI

• Asymmetric lateral habenula function and peripheral neural mechanisms in regulating itch-evoked scratching

  Current Biology · 2025-11-24 · 1 citations

  articleOpen access
  PublisherOA PDFDOI

• Asymmetric Lateral Habenula Function and Peripheral Neural Mechanisms in Regulating Itch-Evoked Scratching

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Effects of different exercise interventions on bone mineral density in elderly postmenopausal women: a network meta-analysis

  Frontiers in Physiology · 2025-09-25 · 2 citations

  reviewOpen access1st authorCorresponding

  Background: Various exercise interventions have been widely applied to enhance site-specific bone mineral density in menopausal females. This network meta-analysis aims to assess and compare the impact of these interventions on improving BMD in this demographic. Methods: A systematic search of PubMed, EMBASE, Cochrane Library, and Web of Science was made up to 4 December 2024 to detect randomized controlled trials (RCTs) comparing continuous endurance training whole-body vibration resistance training multicomponent training mind-body training intermittent training and combined training against control interventions. Primary outcomes included lumbar spine bone mineral density and femoral neck bone mineral density while secondary outcomes covered whole body bone mineral density and total hip bone mineral density A Bayesian random-effects NMA was performed. Results: Fifty-five RCTs involving 3,453 participants were included. Compared with the control group, MCT demonstrated greater efficacy in improving FNBMD (mean difference [MD] 0.02; 95% credible interval [CrI] [0.01, 0.04]). Based on the surface under the cumulative ranking (SUCRA), MBT ranked highest for LSBMD (75.9%), CT for WBBMD (77.6%), and MBT for THBMD (60.7%), suggesting potential benefits of these interventions. Conclusion: This study suggests that MBT, MCT, and CT may contribute to improving BMD in elderly postmenopausal women. However, further rigorously designed RCTs are warranted to validate these findings. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42025636067.

  PublisherOA PDFDOI

• Discovery and biological evaluation of hederagenin derivatives as non-substrate inhibitors of P-glycoprotein-mediated multidrug resistance

  European Journal of Medicinal Chemistry · 2025-02-20 · 1 citations

  review
  PublisherDOI

• Dopaminergic signaling to ventral striatum neurons initiates sniffing behavior

  Nature Communications · 2025-01-02 · 13 citations

  articleOpen access

  Sniffing is a motivated behavior displayed by nearly all terrestrial vertebrates. While sniffing is associated with acquiring and processing odors, sniffing is also intertwined with affective and motivated states. The systems which influence the display of sniffing are unclear. Here, we report that dopamine release into the ventral striatum in mice is coupled with bouts of sniffing and that stimulation of dopaminergic terminals in these regions drives increases in respiratory rate to initiate sniffing whereas inhibition of these terminals reduces respiratory rate. Both the firing of individual neurons and the activity of post-synaptic D1 and D2 dopamine receptor-expressing neurons are coupled with sniffing and local antagonism of D1 and D2 receptors squelches sniffing. Together, these results support a model whereby sniffing can be initiated by dopamine’s actions upon ventral striatum neurons. The nature of sniffing being integral to both olfaction and motivated behaviors implicates this circuit in a wide array of functions. Neural circuitry mechanism which invigorates an animal to go from basal breathing which serves the purpose of gas exchange, to engage in the voluntary act of sniffing is not fully understood. These results from Johnson and colleagues support a model whereby sniffing can be initiated by dopamine’s actions upon ventral striatum neurons.

  PublisherOA PDFDOI

• Therapeutic potential of rutin in premenstrual depression: evidence from in vivo and in vitro studies

  Frontiers in Pharmacology · 2025-01-14 · 4 citations

  articleOpen access

  Introduction Premenstrual dysphoric disorder (PMDD) is a cyclical mood disorder that severely affects the daily life of women of reproductive age. Most of the medications being used clinically have limitations such as low efficacy, side effects, and high cost, so there is an urgent need to discover safer and more effective medications. Rutin is a natural flavonol glycoside with various pharmacological properties including antidepressant. The study of the efficacy and mechanism of action of rutin in PMDD-depressed subtype model rats plays an important role in the discovery of new drugs for the treatment of PMDD. Methods Binding of rutin to gamma-aminobutyric acid type A receptors (GABA A receptors) was probed using molecular docking, microscale thermophoresis, radioactive receptor ligand binding assay and cell membrane clamp experiment. Behavioral tests in mice were performed to screen the optimal dose of rutin. Behavioral tests were performed to evaluate the effects of rutin on depressed mood, memory impairment, and social impairment in PMDD-depressed subtype model rats. HE staining and Golgi staining were performed to observe the neuronal damage in rat hippocampus. UHPLC-MS/MS targeted metabolomics was performed to detect the changes of neurotransmitter content in rat hippocampus. PCR array to detect the effect of rutin on mRNA expression of GABA A receptor partial subunits in rat hippocampus. Results The docking score of rutin with the GABA A receptor benzodiazepine site was −11.442 and the gliding score was −11.470. The Kd of rutin with the GABA A receptor (α1β2γ2) was 1.17 ± 0.89 μM. Rutin competed with [H 3 ]-flunitrazepam for the GABA A receptor benzodiazepine site and inhibited the inward flow of chloride ions ( P < 0.05). In PMDD-depressed subtype rats, rutin alleviated depressed mood, memory impairment and social impairment, ameliorated hippocampal neuronal damage and reduces gamma-aminobutyric acid (GABA) and acetylcholine (ACh) levels ( P < 0.05). Moreover, we found that rutin did not affect the relative mRNA expression of GABA A receptor subunits in rat hippocampus. Discussion Overall, rutin alleviated depressed mood, memory impairment and social impairment in PMDD-depressed subtype rats, which may be related to binding to GABA A receptor benzodiazepine sites, inhibiting chloride ions inward flow, ameliorating hippocampal neuronal damage and reducing GABA and ACh levels. The results of this study provide an experimental basis and scientific evidence for the development of new drugs for the treatment of PMDD.

  PublisherOA PDFDOI

Recent grants

• Circuitry and function of ventral striatum subregions

  NIH · $2.1M · 2020–2026

• NIH Grant R03DC005127

  NIH · $242k · 2005

• US-French Research Proposal: Collaborative Research: Predicting Odorant-dependent and Independent Olfactory Neuron Activation Based on Receptor

  NSF · $154k · 2015–2018

• NIH Grant R55DC006213

  NIH · $100k · 2005

• Novel Role of a Ventral Striatal Circuit in Motor Control

  NIH · $2.4M · 2021–2027

Frequent coauthors

• Janardhan P. Bhattarai

  University of Pennsylvania

  40 shared

• Daniel W. Wesson

  Florida College

  36 shared

• Wenqin Luo

  27 shared

• Yun Feng Zhang

  University of Otago

  26 shared

• Xavier Grosmaître

  Centre des Sciences du Goût et de l'Alimentation

  24 shared

• Hiroaki Matsunami

  Duke University

  20 shared

• Huikai Tian

  University of Pennsylvania

  19 shared

• Marc V. Fuccillo

  University of Pennsylvania

  18 shared

Labs

• Minghong Ma LabPI

Education

• Postdoc, Neurobiology

  Yale University

  2002

• Ph.D., Center for Neurobiology and Behavior

  Columbia University

  1997

• M.S., Biophysics

  Chinese Academy of Sciences

  1991

• B.S., Biophysics

  Peking University

  1988