Clifford Woolf

Clifford Woolf, MB, BCh, PhD

Professor of Neurology, Harvard Medical School

Adaptive and Maladaptive Plasticity in Sensory and Motor Systems

Neurons are subject to functional, chemical and structural plasticity. This plasticity is an important factor both in the normal function of the nervous system and in a vast range of neurological diseases.

The Woolf lab studies how different forms of neuronal plasticity contribute both to adaptive and maladaptive changes in the mammalian nervous system, particularly in relation to pain, regeneration and neurodegenerative diseases.

Most of our work is concentrated on primary sensory and motor neurons, and to the interaction of neurons and immune cells, using a multidisciplinary approach spanning stem cell, molecular and cell biology, electrophysiology, neuroanatomy, behavior and genetics. We have established functional and comparative genomic strategies using expression profiling, bioinformatics and gain- and loss-of-function approaches, to screen for novel genes that contribute to neuronal plasticity and disease phenotypes. Our group works closely with many academic groups and the pharmaceutical industry to model disease and identify molecular targets for novel analgesics, axonal growth determinants and neuroprotective agents.

Current research includes study of the transcriptional control and post-translational processing of receptors and ion channels that mediate pain hypersensitivity, selective silencing of defined neuronal populations, intracellular signal transduction cascades activated by peripheral inflammation and nerve injury, neuro-immune interactions, transcription factors as master regulators of pain, growth and survival programs, cell survival in injured sensory and motor neurons, and the contribution of intrinsic growth determinants in establishing regenerative capacity in the peripheral and central nervous system. We are an active part of the Harvard Stem Cell Institute and are investigating how sensory and motor neurons reprogrammed from patient fibroblasts can be used to study pain and motor neuron disease and to screen for new treatments.

Publications View
Cell Rep
Authors: Authors: Sensory neurons display cell-type-specific vulnerability to loss of neuron-glia interactions
2022 Jul 19; 40(3):111130.
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Exp Neurol
Authors: Authors: The downregulation of GAP-43 is not responsible for the failure of regeneration in freeze-killed nerve grafts in the rat
1994 Oct; 129(2):311-20.
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Neuroscience
Authors: Authors: Time-dependent differences in the increase in GAP-43 expression in dorsal root ganglion cells after peripheral axotomy
1991; 45(1):213-20.
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Neurosci Lett
Authors: Authors: Neurogenic extravasation and substance P levels are low in muscle as compared to skin the rat hindlimb
1984 Dec 21; 52(3):235-40.
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S Afr Med J
Authors: Authors: Management of acute traumatic pain by peripheral transcutaneous electrical stimulation
1977 Aug 13; 52(8):309-12.
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J Neurophysiol
Authors: Authors: Small-caliber afferent inputs produce a heterosynaptic facilitation of the synaptic responses evoked by primary afferent A-fibers in the neonatal rat spinal cord in vitro
1993 Jun; 69(6):2116-28.
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Neurosci Lett
Authors: Authors: An intracellular analysis of amino acid induced excitations of deep dorsal horn neurones in the rat spinal cord slice
1988 Jul 08; 89(3):286-92.
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1982 Mar 17; 29(1):67-72.
Authors: Authors: Do opioid peptides mediate a presynaptic control of C-fibre transmission in the rat spinal cord? Neurosci Lett

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1995 Apr; 74(4):396-9.
Authors: Authors: Is there any clinical advantage of increasing the pre-emptive dose of morphine or combining pre-incisional with postoperative morphine administration? Br J Anaesth

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Eur J Neurosci
Authors: Authors: GAP-43 mRNA in Rat Spinal Cord and Dorsal Root Ganglia Neurons: Developmental Changes and Re-expression Following Peripheral Nerve Injury
1992; 4(10):883-95.
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