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
Lancet
Authors: Authors: Preoperative morphine pre-empts postoperative pain
1993 Jul 10; 342(8863):73-5.
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Neuroscience
Authors: Authors: The responses recorded in vitro of deep dorsal horn neurons to direct and orthodromic stimulation in the young rat spinal cord
1988 Oct; 27(1):231-42.
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Brain Res
Authors: Authors: Chronic peripheral nerve section diminishes the primary afferent A-fibre mediated inhibition of rat dorsal horn neurones
1982 Jun 17; 242(1):77-85.
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Pain
Authors: Authors: Noxious stimuli induce an N-methyl-D-aspartate receptor-dependent hypersensitivity of the flexion withdrawal reflex to touch: implications for the treatment of mechanical allodynia
1995 Jun; 61(3):383-390.
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Nature
Authors: Authors: Peripheral nerve injury triggers central sprouting of myelinated afferents
1992 Jan 02; 355(6355):75-8.
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Neuroscience
Authors: Authors: The brief and the prolonged facilitatory effects of unmyelinated afferent input on the rat spinal cord are independently influenced by peripheral nerve section
1986 Apr; 17(4):1199-205.
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Pain
Authors: Authors: Antinociceptive effect of peripheral segmental electrical stimulation in the rat
1980 Apr; 8(2):237-252.
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Eur J Med Chem
Authors: Authors: Development of a PET radioligand for a2d-1 subunit of calcium channels for imaging neuropathic pain
2022 Nov 15; 242:114688.
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J Comp Neurol
Authors: Authors: Cobalt accumulation in neurons expressing ionotropic excitatory amino acid receptors in young rat spinal cord: morphology and distribution
1994 Jun 15; 344(3):321-35.
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Neuroscience
Authors: Authors: The growth-associated protein GAP-43 appears in dorsal root ganglion cells and in the dorsal horn of the rat spinal cord following peripheral nerve injury
1990; 34(2):465-78.
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