Nervous System Plasticity and Chronic Pain

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Physiological characterization of spinal lamina I projection neurons in rats with unilateral adjuvant-induced inflammation, submitted Google Scholar.

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Differential activation of spinal cord dynorphin and enkephalin neurons during hyperalgesia: evidence using cDNA hybridization. Pathophysiology of nerve following mechanical injury. Amsterdam: Elsevier. The effect of carrageenan-induced inflammation on the sensitivity of unmyelinated skin nociceptors in the rat.

Peripheral neural mechanisms of cutaneous hyperalgesia following mild injury by heat.

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Changes in the somatotopic organization of the cat lumbar spinal cord following peripheral nerve transection and regeneration. Saphenous has weak ineffective synapses in sciatic territory of rat spinal cord: electrical stimulation of the saphenous or application of drugs reveal these somatotopically inappropriate synapses.

Frontiers | Reward Circuitry Plasticity in Pain Perception and Modulation | Pharmacology

Receptive fields of rat lamina I projection cells move to incorporate a nearby region of injury. Properties of synaptic linkage from long ranging afferents onto dorsal horn neurons in normal and deafferented cats. Electrophysiological characteristics of dorsal horn cells in rats with cutaneous inflammation resulting from chronic arthritis. Factors forming the edge of a receptive field: the presence of relatively ineffective afferent terminals.

A model of chronic pain in the rat: Response of multiple opioid systems to adjuvant-induced arthritis. Release of substance P from the spinal dorsal horn is enhanced in polyarthritic rats. The boundary of proximal hindlimb representation in the dorsal horn following peripheral nerve lesions in cats: a reevaluation of plasticity in the somatotopic map. Electrical stimulation reveals relatively ineffective sural nerve projections to dorsal horn neurons in the cat.

Evidence for different mechanisms of primary and secondary hyperalgesia following heat injury to the glabrous skin. Does neurogenic inflammation alter the sensitivity of unmyelinated nociceptors in the rat?

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Absence of intraspinal sprouting in dorsal root axons caudal to a partial spinal hemisection: a horseradish peroxidase transport study. An examination of intraspinal sprouting in dorsal root axons with the tracer horseradish peroxidase. Actions of calcitonin gene-related peptide on rat spinal dorsal horn neurons.

Effects of 4-amino-pyridine, GAB A and bicuculline on cutaneous receptive fields of cat dorsal horn neurons.

Direct observation of the sensitization of articular afferents during an experimental arthritis. Effect of nerve section on the spinal distribution of neighboring nerves. Plasticity of somatosensory maps in the adult mammalian spinal cord.

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Slow excitatory transmission in rat dorsal horn: possible mediation by peptides. The effect of peripheral nerve injury on dorsal root potentials and on transmission of afferent signals into the spinal cord. The response of rat spinal cord cells to unmyelinated afferents after peripheral nerve section and after changes in substance P levels.

Brain Changes in Chronic Pain Patients

Action of picrotoxin upon trigeminal subnucleus caudalis neurons in the monkey. Ethical guidelines for investigations of experimental pain in conscious animals. Dubner 1 J. Hylden 1 R. Nahin 1 R. Traub 1 1. Paradoxically, such nociception is often followed by prolonged analgesia attenuating pre-existing persistent pain.

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Topical capsaicin has been approved by the FDA for treatment of post-herpetic neuralgia, and provides months-long relief. However, the mechanisms underlying capsaicin-induced analgesia are not well understood. We also found that local pharmacological inhibition of TRPV1 at the central terminals of primary afferents was sufficient to attenuate mechanical hyperalgesia and allodynia.

The goal of this project is to elucidate how pain receptor TRPV1 contributes to chronic pain under pathological conditions.

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This is an important step for the development of novel therapeutics targeting the pain receptor TRPV1 and nerves expressing TRPV1 more specifically with fewer side effects for suppressing pathological pain. Toggle navigation.

Edited by Eduardo Benarroch

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