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
Neurosci Lett
Authors: Authors: Regional differences in the distribution of capsaicin-sensitive target-identified adult rat dorsal root ganglion neurons
1992 Aug 31; 143(1-2):251-4.
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J Neurosci
Authors: Authors: Relative effectiveness of C primary afferent fibers of different origins in evoking a prolonged facilitation of the flexor reflex in the rat
1986 May; 6(5):1433-42.
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Brain Res
Authors: Authors: Analgesia and hyperalgesia produced in the rat by intrathecal naloxone
1980 May 12; 189(2):593-7.
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Sci Transl Med
Authors: Authors: Phenotypic drug screen uncovers the metabolic GCH1/BH4 pathway as key regulator of EGFR/KRAS-mediated neuropathic pain and lung cancer
2022 08 31; 14(660):eabj1531.
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J Neurophysiol
Authors: Authors: The contribution of GABAA and glycine receptors to central sensitization: disinhibition and touch-evoked allodynia in the spinal cord
1994 Jul; 72(1):169-79.
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Eur J Neurosci
Authors: Authors: Activity-Dependent Changes in Rat Ventral Horn Neurons in vitro; Summation of Prolonged Afferent Evoked Postsynaptic Depolarizations Produce a d-2-Amino-5-Phosphonovaleric Acid Sensitive Windup
1990; 2(7):638-49.
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Neurosci Lett
Authors: Authors: A selective effect of naloxone on heterosynaptic C-fibre-mediated inhibitions in the rat dorsal horn
1984 Mar 23; 45(2):169-74.
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Neuropharmacology
Authors: Authors: Pyrogen and prostaglandin fever in the rabbit-II: Effects of noradrenaline depletion and adrenergic receptor blockade
1975 May-Jun; 14(5-6):405-11.
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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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