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
Influence of inflammation or disconnection from peripheral target tissue on the capsaicin sensitivity of rat dorsal root ganglion sensory neurones.
Authors: Authors: Hu-Tsai M, Woolf C, Winter J.
Neurosci Lett
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Overcoming inhibition
Authors: Authors: Spinal injury
Nature
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Prevention or elimination of central sensitization
Authors: Authors: A new strategy for the treatment of inflammatory pain
Drugs
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Neuroscience
Authors: Authors: The role of neurokinin and N-methyl-D-aspartate receptors in synaptic transmission from capsaicin-sensitive primary afferents in the rat spinal cord in vitro
1993 Feb; 52(4):1029-37.
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Neurosci Lett
Authors: Authors: Excitatory amino acids increase glycogen phosphorylase activity in the rat spinal cord
1987 Jan 27; 73(3):209-14.
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Brain Res
Authors: Authors: Inhibitory controls on thermal neurones in the spinal trigeminal nucleus of cats and rats
1981 Mar 30; 209(2):440-5.
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Nat Commun
Authors: Authors: Transcription factor network analysis identifies REST/NRSF as an intrinsic regulator of CNS regeneration in mice
2022 07 29; 13(1):4418.
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Neuroreport
Authors: Authors: NK1 and NK2 receptors contribute to C-fibre evoked slow potentials in the spinal cord
1994 Oct 27; 5(16):2105-8.
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Trends Neurosci
Authors: Authors: Common patterns of plasticity contributing to nociceptive sensitization in mammals and Aplysia
1991 Feb; 14(2):74-8.
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J Comp Neurol
Authors: Authors: The somatotopic organization of primary afferent terminals in the superficial laminae of the dorsal horn of the rat spinal cord
1985 Jan 01; 231(1):66-77.
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