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
J Physiol
Authors: Authors: Muscle but not cutaneous C-afferent input produces prolonged increases in the excitability of the flexion reflex in the rat
1984 Nov; 356:443-58.
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J Physiol
Authors: Authors: A dissociation between temperature regulation and fever in the rabbit
1977 Apr; 266(2):423-33.
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J Neurophysiol
Authors: Authors: Rate of rise of the cumulative depolarization evoked by repetitive stimulation of small-caliber afferents is a predictor of action potential windup in rat spinal neurons in vitro
1993 May; 69(5):1621-31.
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J Physiol (Paris)
Authors: Authors: Prolonged primary afferent induced alterations in dorsal horn neurones, an intracellular analysis in vivo and in vitro
1988-1989; 83(3):255-66.
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Neuroscience
Authors: Authors: The time course and specificity of the changes in the behavioural and dorsal horn cell responses to noxious stimuli following peripheral nerve capsaicin treatment in the rat
1982; 7(9):2051-6.
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Anaesthesia
Authors: Authors: Pre-emptive analgesia
1995 Feb; 50(2):176-7.
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J Neurocytol
Authors: Authors: Terminal Schwann cells elaborate extensive processes following denervation of the motor endplate
1992 Jan; 21(1):50-66.
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Pain
Authors: Authors: The systemic administration of local anaesthetics produces a selective depression of C-afferent fibre evoked activity in the spinal cord
1985 Dec; 23(4):361-374.
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Pain
Authors: Authors: Transcutaneous electrical nerve stimulation and the reaction to experimental pain in human subjects
1979 Oct; 7(2):115-127.
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Dis Model Mech
Authors: Authors: Bortezomib-induced neurotoxicity in human neurons is the consequence of nicotinamide adenine dinucleotide depletion
2022 Nov 18.
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