David D Ginty

David D Ginty, Ph.D.

Edward R. and Anne G. Lefler Professor of Neurobiology, Harvard Medical School
Head of the Department of Neurobiology, Harvard Medical School

Neurons and Circuits That Mediate Touch

The somatosensory system endows us with a remarkable capacity for recognizing textural differences and shapes of objects held in our hands, and to feel pain, pressure, temperature, position, movement and vibration. Understanding the neurobiological basis of touch perception will help us to determine why touch can be painful or aversive under certain pathological states.

The Ginty lab uses mouse molecular genetics, in vitro signaling approaches, circuit mapping, electrophysiological and behavioral analyses to gain understanding of the development, organization, and function of neural circuits that underlie the sense of touch. Mouse molecular genetic approaches are used to identify, visualize, and functionally manipulate physiologically defined classes of low-threshold mechanosensory neurons (LTMRs) and nociceptors, the primary cutaneous sensory neurons that mediate the sense of touch and pain. We also strive to gain genetic access to spinal cord interneurons and projection neurons to reveal the organizational logic and functions of touch and pain circuits in the spinal cord and brainstem.

Our current goals are to discover: 1) the unique functions and properties of LTMR and nociceptor subtypes; 2) the organization of synaptic connections between LTMR subtypes and nociceptors, spinal cord dorsal horn interneurons and projection neurons, and dorsal column nuclei neurons; 3) the neural circuits that underlie the perception of touch; 4) molecular and developmental mechanisms by which primary somatosensory neurons and touch and pain circuit organization are established; and 5) mechanisms of touch circuit dysfunction in mouse models of autism spectrum disorders and neuropathic pain.

Publications View
An NGF-TrkA-mediated retrograde signal to transcription factor CREB in sympathetic neurons.
Authors: Authors: Riccio A, Pierchala BA, Ciarallo CL, Ginty DD.
Science
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Coupling of the RAS-MAPK pathway to gene activation by RSK2, a growth factor-regulated CREB kinase.
Authors: Authors: Xing J, Ginty DD, Greenberg ME.
Science
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Calcium activates serum response factor-dependent transcription by a Ras- and Elk-1-independent mechanism that involves a Ca2+/calmodulin-dependent kinase.
Authors: Authors: Miranti CK, Ginty DD, Huang G, Chatila T, Greenberg ME.
Mol Cell Biol
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Serine 133-phosphorylated CREB induces transcription via a cooperative mechanism that may confer specificity to neurotrophin signals.
Authors: Authors: Bonni A, Ginty DD, Dudek H, Greenberg ME.
Mol Cell Neurosci
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L-type voltage-sensitive Ca2+ channel activation regulates c-fos transcription at multiple levels.
Authors: Authors: Thompson MA, Ginty DD, Bonni A, Greenberg ME.
J Biol Chem
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Membrane depolarization and calcium influx stimulate MEK and MAP kinase via activation of Ras.
Authors: Authors: Rosen LB, Ginty DD, Weber MJ, Greenberg ME.
Neuron
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A growth factor-induced kinase phosphorylates the serum response factor at a site that regulates its DNA-binding activity.
Authors: Authors: Rivera VM, Miranti CK, Misra RP, Ginty DD, Chen RH, Blenis J, Greenberg ME.
Mol Cell Biol
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Regulation of gene expression in hippocampal neurons by distinct calcium signaling pathways.
Authors: Authors: Bading H, Ginty DD, Greenberg ME.
Science
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Trans-synaptic regulation of gene expression.
Authors: Authors: Ginty DD, Bading H, Greenberg ME.
Curr Opin Neurobiol
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The activity of cAMP-dependent protein kinase is required at a posttranslational level for induction of voltage-dependent sodium channels by peptide growth factors in PC12 cells.
Authors: Authors: Ginty DD, Fanger GR, Wagner JA, Maue RA.
J Cell Biol
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