A5036506943- Pain Mechanisms and Treatments
- Nerve injury and regeneration
- Neuropeptides and Animal Physiology
- Neurogenesis and neuroplasticity mechanisms
- Ion channel regulation and function
- Urinary Bladder and Prostate Research
- Neuroscience and Neuropharmacology Research
- Axon Guidance and Neuronal Signaling
- Botulinum Toxin and Related Neurological Disorders
- Spinal Cord Injury Research
- Neuroscience and Neural Engineering
- Adenosine and Purinergic Signaling
- Pain Management and Placebo Effect
- Neuroscience of respiration and sleep
- Musculoskeletal pain and rehabilitation
- Nerve Injury and Rehabilitation
- Ion Channels and Receptors
- Pediatric Pain Management Techniques
- Transcranial Magnetic Stimulation Studies
- Stress Responses and Cortisol
- Exercise and Physiological Responses
- Dermatology and Skin Diseases
- Pain Management and Opioid Use
- Hereditary Neurological Disorders
- Migraine and Headache Studies
King's College London
2016-2025
Wake Forest University
2022
Wolfson Foundation
2014-2021
Wellcome Trust
2020
University College London
1983-2016
University of London
2016
King's College - North Carolina
2000-2016
University of Minnesota
2015
University of Pennsylvania
2015
Imperial College London
2002-2015
Abstract Immunocytochemistry has been used to examine the location of trkA, high‐affinity receptor for nerve growth factor, in adult rat dorsal root ganglia, trigeminal ganglia and spinal cord. TrkA immunoreactivity was observed small medium sized ganglion cells horn In lumbar L4 L5 trkA‐immunoreactive constitute 40% range size from 15 45 μm diameter. Double labelling using markers various subpopulations revealed that virtually all (92%) express calcitonin gene‐related peptide (CGRP)...
Several lines of evidence suggest that neurotrophin administration may be some therapeutic benefit in the treatment peripheral neuropathy. However, a third sensory neurons do not express receptors for neurotrophins. These are small diameter and can identified by binding lectin IB4 expression enzyme thiamine monophosphatase (TMP). Here we show these receptor components glial-derived neurotrophic factor (GDNF) signaling (RET, GFRα-1, GFRα-2). In lumbar dorsal root ganglia, virtually all...
Neuropathic pain arises as a debilitating consequence of nerve injury. The etiology such is poorly understood, and existing treatment largely ineffective. We demonstrate here that glial cell line–derived neurotrophic factor (GDNF) both prevented reversed sensory abnormalities developed in neuropathic models, without affecting pain-related behavior normal animals. GDNF reduces ectopic discharges within neurons after This may arise the reversal by injury-induced plasticity several sodium...
Central sensitization, the hyperexcitability of spinal processing that often accompanies peripheral injury, is a major component many persistent pain states. Here we report neurotrophin, brain-derived neurotrophic factor (BDNF), modulator excitability within cord and contributes to mechanism central sensitization. BDNF, localized in primary sensory neuron cell bodies terminals, potentiates nociceptive reflex responses an vitro preparation induces c-fos expression dorsal horn neurons. NMDA...
Chondroitin sulfate proteoglycans (CSPGs) are inhibitory extracellular matrix molecules that upregulated after CNS injury. Degradation of CSPGs using the enzyme chondroitinase ABC (ChABC) can promote functional recovery spinal cord However, mechanisms underlying this not clear. Here we investigated effects ChABC treatment on promoting plasticity within cord. We found robust sprouting both injured (corticospinal) and intact (serotonergic) descending projections as well uninjured primary...
Extracellular ATP plays a role in nociceptive signalling and sensory regulation of visceral function through ionotropic receptors variably composed P2X2 P2X3 subunits. subunits can form homomultimeric P2X2, P2X3, or heteromultimeric P2X2/3 receptors. However, the relative contribution these receptor subtypes to afferent functions vivo is poorly understood. Here we describe null mutant mice lacking subunit (P2X2-/-) double both (P2X2/P2X3(Dbl-/-)), compare with previously characterized...