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Qiufu Ma, PhD


Researcher

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Qiufu Ma, PhD

Researcher

  • Professor of Neurobiology, Harvard Medical School

Contact Information

  • Office Phone Number(617) 632-4594
  • Fax(617) 632-4595

Bio

Dr. Qiufu Ma received his BS from Fudan University in 1987 and PhD from UCLA in 1994. After postdoctoral training with Dr. David Anderson at Caltech, he became an Assistant Professor at Harvard Neurobiology Department and Dana-Farber Cancer Institute, and become a full Professor in 2011. He was a Pew Scholar from 2000-2004. Since 2007, he has been serving as the Faculty Director of the Office for Postdoctoral Training and Career Development.

Recent Awards:

  • Pew Scholar 2000
  • SCBA Young Investigator Award 2001

Research

Our lab focuses on two lines of research: mapping pain pathways and exploring how acupuncture works. During the past decade, we have been using genetic tools, electrophysiological recordings, and novel behavioral assays to characterize spinal pathways that transmit clinically relevant pain. One key achievement is the identification of spinal neurons that transmit pain evoked by dynamic skin touch, one of most bothersome  forms of pain suffered by patients with nerve injury. More recently, we revealed spinal pathways that drive sustained affective pain caused by severe body injury (e.g., skin burn injury). Importantly, loss of these clinically relevant forms of pain is not detected by reflex-based assays commonly used by the pain field for decades—partly explaining poor translation from preclinical studies to new pain medicines. Currently, the lab is characterizing neural pathways transmitting pain from muscles, bones and visceral organs. Though prevalent and difficult to treat, this type of deep tissue pain is still understudied.
Another insight from past decades’ studies is the realization that there are many redundant neural pathways and mechanisms that can drive pain, making it difficult to develop effective drugs by targeting specific pathways or molecules. A core wisdom of traditional Chinese medicine practices, such as acupuncture, deals with the root of diseases (e.g., inflammation) that drive symptoms like pain. Since 2017, my lab has been studying how stimulation of somatosensory neurons by electroacupuncture drives autonomic nervous reflexes that can in turn modulate local or systemic inflammation; these new studies will explore the modern neuroanatomical basis behind acupuncture practice and help develop new systems biology approaches to treat diseases and chronic pain.

A functional subdivision within the somatosensory system and its implications for pain research. Neuron. 2022 03 02; 110(5):749-769.
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Author Correction: A neuroanatomical basis for electroacupuncture to drive the vagal-adrenal axis. Nature. 2022 Jan; 601(7893):E9.
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A neuroanatomical basis for electroacupuncture to drive the vagal-adrenal axis. Nature. 2021 10; 598(7882):641-645.
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Somato-Autonomic Reflexes of Acupuncture. Med Acupunct. 2020 Dec 01; 32(6):362-366.
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Somatotopic Organization and Intensity Dependence in Driving Distinct NPY-Expressing Sympathetic Pathways by Electroacupuncture. Neuron. 2020 11 11; 108(3):436-450.e7.
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Identifying the pathways required for coping behaviours associated with sustained pain. Nature. 2019 01; 565(7737):86-90.
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Timing Mechanisms Underlying Gate Control by Feedforward Inhibition. Neuron. 2018 09 05; 99(5):941-955.e4.
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Incoherent feed-forward regulatory loops control segregation of C-mechanoreceptors, nociceptors, and pruriceptors. J Neurosci. 2015 Apr 01; 35(13):5317-29.
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Transcriptional profiling at whole population and single cell levels reveals somatosensory neuron molecular diversity. Elife. 2014 Dec 19; 3.
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Identification of spinal circuits transmitting and gating mechanical pain. Cell. 2014 Dec 04; 159(6):1417-1432.
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Merkel cells are a touchy subject. Cell. 2014 Apr 24; 157(3):531-3.
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Genetic control of the segregation of pain-related sensory neurons innervating the cutaneous versus deep tissues. Cell Rep. 2013 Dec 12; 5(5):1353-64.
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Ontogeny of excitatory spinal neurons processing distinct somatic sensory modalities. J Neurosci. 2013 Sep 11; 33(37):14738-48.
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Activity-dependent silencing reveals functionally distinct itch-generating sensory neurons. Nat Neurosci. 2013 Jul; 16(7):910-8.
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Runx1 controls terminal morphology and mechanosensitivity of VGLUT3-expressing C-mechanoreceptors. J Neurosci. 2013 Jan 16; 33(3):870-82.
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Genome-scale study of transcription factor expression in the branching mouse lung. Dev Dyn. 2012 Sep; 241(9):1432-53.
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Tlx3 and Runx1 act in combination to coordinate the development of a cohort of nociceptors, thermoceptors, and pruriceptors. J Neurosci. 2012 Jul 11; 32(28):9706-15.
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TLR3 deficiency impairs spinal cord synaptic transmission, central sensitization, and pruritus in mice. J Clin Invest. 2012 Jun; 122(6):2195-207.
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Identification of molecular compartments and genetic circuitry in the developing mammalian kidney. Development. 2012 May; 139(10):1863-73.
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Population coding of somatic sensations. Neurosci Bull. 2012 Apr; 28(2):91-9.
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Genetic marking and characterization of Tac2-expressing neurons in the central and peripheral nervous system. Mol Brain. 2012 Jan 24; 5:3.
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Phenotypic switching of nonpeptidergic cutaneous sensory neurons following peripheral nerve injury. PLoS One. 2011; 6(12):e28908.
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VGLUT2-dependent glutamate release from nociceptors is required to sense pain and suppress itch. Neuron. 2010 Nov 04; 68(3):543-56.
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Labeled lines meet and talk: population coding of somatic sensations. J Clin Invest. 2010 Nov; 120(11):3773-8.
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Generation of somatic sensory neuron diversity and implications on sensory coding. Curr Opin Neurobiol. 2011 Feb; 21(1):52-60.
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Characterization of two Runx1-dependent nociceptor differentiation programs necessary for inflammatory versus neuropathic pain. Mol Pain. 2010 Jul 30; 6:45.
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Loss of inhibitory interneurons in the dorsal spinal cord and elevated itch in Bhlhb5 mutant mice. Neuron. 2010 Mar 25; 65(6):886-98.
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RETouching upon mechanoreceptors. Neuron. 2009 Dec 24; 64(6):773-6.
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A genome-wide screen for spatially restricted expression patterns identifies transcription factors that regulate glial development. J Neurosci. 2009 Sep 09; 29(36):11399-408.
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JNK-induced MCP-1 production in spinal cord astrocytes contributes to central sensitization and neuropathic pain. J Neurosci. 2009 Apr 01; 29(13):4096-108.
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Acquisition of granule neuron precursor identity is a critical determinant of progenitor cell competence to form Shh-induced medulloblastoma. Cancer Cell. 2008 Aug 12; 14(2):123-34.
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Regulation of motor neuron specification by phosphorylation of neurogenin 2. Neuron. 2008 Apr 10; 58(1):65-77.
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Tlx1 and Tlx3 coordinate specification of dorsal horn pain-modulatory peptidergic neurons. J Neurosci. 2008 Apr 09; 28(15):4037-46.
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Mechanisms of compartmentalized expression of Mrg class G-protein-coupled sensory receptors. J Neurosci. 2008 Jan 02; 28(1):125-32.
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Nociceptors--noxious stimulus detectors. Neuron. 2007 Aug 02; 55(3):353-64.
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Cerebellar 'transcriptome' reveals cell-type and stage-specific expression during postnatal development and tumorigenesis. Mol Cell Neurosci. 2006 Nov; 33(3):247-59.
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Transcriptional regulation of neuronal phenotype in mammals. J Physiol. 2006 Sep 01; 575(Pt 2):379-87.
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Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic pain. Neuron. 2006 Feb 02; 49(3):365-77.
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Lbx1 and Tlx3 are opposing switches in determining GABAergic versus glutamatergic transmitter phenotypes. Nat Neurosci. 2005 Nov; 8(11):1510-5.
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Mouse brain organization revealed through direct genome-scale TF expression analysis. Science. 2004 Dec 24; 306(5705):2255-7.
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Tlx3 and Tlx1 are post-mitotic selector genes determining glutamatergic over GABAergic cell fates. Nat Neurosci. 2004 May; 7(5):510-7.
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Lmx1b, Pet-1, and Nkx2.2 coordinately specify serotonergic neurotransmitter phenotype. J Neurosci. 2003 Nov 05; 23(31):9961-7.
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Proper development of relay somatic sensory neurons and D2/D4 interneurons requires homeobox genes Rnx/Tlx-3 and Tlx-1. Genes Dev. 2002 May 15; 16(10):1220-33.
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