Return to list David Ginty, PhD


David Ginty, PhD

Edward R. and Anne G. Lefler Professor of Neurobiology; Investigator, HHMI



Harvard Medical School
210 Longwood Avenue
Boston, MA 02115






My current and future research addresses the development, organization, and function of neural circuits that underlie the perception of touch and pain. This focus stems naturally from our long-standing effort to define trophic factor signaling mechanisms and axonal guidance cues that orchestrate the assembly of PNS circuits. For our current focus, we have generated more than 50 targeted deletions and alterations of the mouse genome that enable interrogation of the major physiologically distinct classes of low-threshold mechanosensory neurons (LTMRs), which are the primary cutaneous sensory neurons that mediate our sense of touch, as well as nociceptors, which detect painful stimuli. In addition, we have recently produced a complementary set of mouse genetic tools to investigate spinal cord interneuron and projection neuron subtypes. This array of somatosensory nervous system genetic tools enables visualization, targeted in vitro and in vivo electrophysiological recordings, and functional manipulation of LTMRs and nociceptors as well as dorsal horn and brainstem LTMR circuit components that underlie the sense of touch.

We have attempted to incorporate flexibility and adaptability into our scientific approach by developing tools and techniques, especially reverse, forward, and chemical genetic approaches to neurobiological research, and more recently in vivo electrophysiological and behavioral approaches that take advantage of opportunities afforded by our array of somatosensory genetic tools. Our work in this area has so far defined molecular and morphological bases of LTMR subtype response properties, mechanisms of LTMR and nociceptor development, and an appreciation of LTMR circuit organization that provides a conceptual framework for understanding how ensembles of LTMR activity are integrated and processed in the CNS, and a spinal cord locus of dysfunction that underlies tactile processing deficits in animal models of autism spectrum disorders (ASD). Our current work employs a multidisciplinary approach to address: 1) the morphological and molecular basis of LTMR and nociceptor subtype response properties; 2) the organization, development and function of innocuous touch circuits in the spinal cord dorsal horn, and dorsal horn projection neurons; and 3) the cellular and molecular basis, and behavioral consequences, of LTMR circuit dysfunction in mouse models of pervasive developmental disorders. This is an exciting period because of the tremendous opportunity, enabled by our unique LTMR, nociceptor, and spinal cord genetic toolbox and powerful electrophysiological, anatomical, and behavioral techniques, to address fundamental and relatively unexplored areas of somatosensory research.

Understanding somatosensation deficits in ASD - Simons Foundation, 345690