about
Retinoids activate the irritant receptor TRPV1 and produce sensory hypersensitivityDeterminants of TRPV4 activity following selective activation by small molecule agonist GSK1016790A.Long-lasting synaptic potentiation induced by depolarization under conditions that eliminate detectable Ca2+ signals.Peripheral injury induces long-term sensitization of defensive responses to visual and tactile stimuli in the squid Loligo pealeii, Lesueur 1821.Transformation of siphon responses during conditioning of Aplysia suggests a model of primitive stimulus-response associationSquid have nociceptors that display widespread long-term sensitization and spontaneous activity after bodily injuryMechanosensory neurons innervating Aplysia siphon encode noxious stimuli and display nociceptive sensitization.Chronic spontaneous activity generated in the somata of primary nociceptors is associated with pain-related behavior after spinal cord injury.Spinal cord injury triggers an intrinsic growth-promoting state in nociceptorsPersistent Electrical Activity in Primary Nociceptors after Spinal Cord Injury Is Maintained by Scaffolded Adenylyl Cyclase and Protein Kinase A and Is Associated with Altered Adenylyl Cyclase Regulation.Long-lasting hyperexcitability induced by depolarization in the absence of detectable Ca2+ signals.Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathyTargeting Pain-evoking Transient Receptor Potential Channels for the Treatment of Pain.Molluscan memory of injury: evolutionary insights into chronic pain and neurological disorders.Neuroinflammatory contributions to pain after SCI: roles for central glial mechanisms and nociceptor-mediated host defense.Long-term alterations induced by injury and by 5-HT in Aplysia sensory neurons: convergent pathways and common signals?Injury-related behavior and neuronal plasticity: an evolutionary perspective on sensitization, hyperalgesia, and analgesia.Priming events and retrograde injury signals. A new perspective on the cellular and molecular biology of nerve regeneration.Modulation of mechanosensory threshold in Aplysia by serotonin, small cardioactive peptideB (SCPB), FMRFamide, acetylcholine, and dopamine.Site-specific sensitization of defensive reflexes in Aplysia: a simple model of long-term hyperalgesia.Associative learning in Aplysia: cellular correlates supporting a conditioned fear hypothesis.Axoplasm enriched in a protein mobilized by nerve injury induces memory-like alterations in Aplysia neurons.Defensive responses of larval Manduca sexta and their sensitization by noxious stimuli in the laboratory and field.Persistent pain after spinal cord injury is maintained by primary afferent activity.Nociceptors as chronic drivers of pain and hyperreflexia after spinal cord injury: an adaptive-maladaptive hyperfunctional state hypothesis.Limited contributions of serotonin to long-term hyperexcitability of Aplysia sensory neurons.The use of elevated divalent cation solutions to isolate monosynaptic components of sensorimotor connections in Aplysia.TRPV1 channels make major contributions to behavioral hypersensitivity and spontaneous activity in nociceptors after spinal cord injury.Rapid electrical and delayed molecular signals regulate the serum response element after nerve injury: convergence of injury and learning signals.A neuronal isoform of protein kinase G couples mitogen-activated protein kinase nuclear import to axotomy-induced long-term hyperexcitability in Aplysia sensory neurons.Memory-like alterations in Aplysia axons after nerve injury or localized depolarization.cAMP and cGMP contribute to sensory neuron hyperexcitability and hyperalgesia in rats with dorsal root ganglia compression.Nociceptive sensitization reduces predation risk.Zinc Inhibits TRPV1 to Alleviate Chemotherapy-Induced Neuropathic Pain.Evidence that long-term hyperexcitability of the sensory neuron soma induced by nerve injury in Aplysia is adaptive.Somatotopic organization and functional properties of mechanosensory neurons expressing sensorin-A mRNA in Aplysia californica.Comparative analysis of hyperexcitability and synaptic facilitation induced by nerve injury in two populations of mechanosensory neurones of Aplysia californica.Slow depolarization produced by associative conditioning of Aplysia sensory neurons may enhance Ca2+ entry.Role of peri-axonal inflammation in the development of thermal hyperalgesia and guarding behavior in a rat model of neuropathic pain.Associative Learning in Aplysia: evidence for conditioned fear in an invertebrate.
P50
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P50
description
hulumtues
@sq
researcher
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wetenschapper
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հետազոտող
@hy
name
Edgar T Walters
@ast
Edgar T Walters
@en
Edgar T Walters
@es
Edgar T Walters
@nl
Edgar T Walters
@sl
type
label
Edgar T Walters
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Edgar T Walters
@en
Edgar T Walters
@es
Edgar T Walters
@nl
Edgar T Walters
@sl
prefLabel
Edgar T Walters
@ast
Edgar T Walters
@en
Edgar T Walters
@es
Edgar T Walters
@nl
Edgar T Walters
@sl
P106
P21
P2798
P31
P496
0000-0003-0718-102X