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
Br J Pharmacol
Authors: Authors: Sigma-1 receptor curtails endogenous opioid analgesia during sensitization of TRPV1 nociceptors
2022 Dec 07.
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Curr Opin Neurobiol
Authors: Authors: Reciprocal Schwann cell-axon interactions
1993 Oct; 3(5):683-93.
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Br J Anaesth
Authors: Authors: Recent advances in the pathophysiology of acute pain
1989 Aug; 63(2):139-46.
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Nature
Authors: Authors: Endogenous opioid peptides and pain mechanisms: a complex relationship
1983 Dec 22-1984 Jan 4; 306(5945):739-40.
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J Physiol
Authors: Authors: Proceedings: A role for noradrenaline and cyclic AMP in prostaglandin E1 Fever
1974 Jul; 240(2):49P-50P.
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J Physiol
Authors: Authors: Involvement of neurokinin receptors in the induction but not the maintenance of mechanical allodynia in rat flexor motoneurones
1995 Aug 01; 486 ( Pt 3):769-77.
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Neurosci Lett
Authors: Authors: Neurotoxic damage evokes regenerative responses from adult rat sensory neurones
1992 Oct 26; 146(1):48-52.
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J Comp Neurol
Authors: Authors: Somatotopic organization of cutaneous afferent terminals and dorsal horn neuronal receptive fields in the superficial and deep laminae of the rat lumbar spinal cord
1986 Sep 22; 251(4):517-31.
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Nature
Authors: Authors: What we don't know about pain
1980 Sep 18; 287(5779):185-6.
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J Pain
Authors: Authors: Optimizing and Accelerating the Development of Precision Pain Treatments for Chronic Pain: IMMPACT Review and Recommendations
2022 Oct 02.
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