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 Neurosci
Authors: Authors: Denervation of the motor endplate results in the rapid expression by terminal Schwann cells of the growth-associated protein GAP-43
1992 Oct; 12(10):3999-4010.
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Neurosci Lett
Authors: Authors: Substance P and calcitonin gene-related peptide synergistically modulate the gain of the nociceptive flexor withdrawal reflex in the rat
1986 May 15; 66(2):226-30.
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Brain Res
Authors: Authors: Intracerebral naloxone and the reaction to thermal noxious stimulation in the rat
1980 May 26; 190(2):578-83.
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Front Pain Res (Lausanne)
Authors: Authors: Pain modulation in the spinal cord
2022; 3:984042.
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J Neurosci
Authors: Authors: GAP-43 expression in primary sensory neurons following central axotomy
1994 Jul; 14(7):4375-84.
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J Comp Neurol
Authors: Authors: Neonatal capsaicin treatment induces invasion of the substantia gelatinosa by the terminal arborizations of hair follicle afferents in the rat dorsal horn
1990 Jun 01; 296(1):23-31.
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Pain
Authors: Authors: Long term alterations in the excitability of the flexion reflex produced by peripheral tissue injury in the chronic decerebrate rat
1984 Apr; 18(4):325-343.
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Neuropharmacology
Authors: Authors: The effect of sodium salicylate on dibutyryl cyclic AMP fever in the conscious rabbit
1976 Jan; 15(1):9-10.
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Pain
Authors: Authors: Lignocaine selectively reduces C fibre-evoked neuronal activity in rat spinal cord in vitro by decreasing N-methyl-D-aspartate and neurokinin receptor-mediated post-synaptic depolarizations; implications for the development of novel centrally acting analgesics
1996 Jan; 64(1):59-70.
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J Comp Neurol
Authors: Authors: Morphology and somatotopy of the central arborizations of rapidly adapting glabrous skin afferents in the rat lumbar spinal cord
1993 Mar 22; 329(4):491-511.
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