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
Am J Physiol
Authors: Authors: Hypothalamic heating and cooling in monoamine-depleted rabbits
1975 Feb; 228(2):569-74.
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Br J Pharmacol
Authors: Authors: Contribution of interleukin-1 beta to the inflammation-induced increase in nerve growth factor levels and inflammatory hyperalgesia
1995 Aug; 115(7):1265-75.
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Restor Neurol Neurosci
Authors: Authors: Factors controlling the expression of GAP-43 in dorsal root ganglia cells: implications for plasticity and growth of central terminals
1993 Jan 01; 5(1):51-2.
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Adv Tech Stand Neurosurg
Authors: Authors: Physiological, inflammatory and neuropathic pain
1987; 15:39-62.
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J Physiol
Authors: Authors: The effect of intracerebroventricular injections of morphine on vasopressin release in the rat
1981 Feb; 311:401-9.
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Neuron
Authors: Authors: Core transcription programs controlling injury-induced neurodegeneration of retinal ganglion cells
2022 08 17; 110(16):2607-2624.e8.
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Neuroscience
Authors: Authors: Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity
1994 Sep; 62(2):327-31.
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J Comp Neurol
Authors: Authors: Collateral sprouting of the central terminals of cutaneous primary afferent neurons in the rat spinal cord: pattern, morphology, and influence of targets
1990 Oct 15; 300(3):370-85.
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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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