about
Selective spider toxins reveal a role for the Nav1.1 channel in mechanical painMultiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.α-Conotoxin Vc1.1 inhibits human dorsal root ganglion neuroexcitability and mouse colonic nociception via GABAB receptors.Identifying unique subtypes of spinal afferent nerve endings within the urinary bladder of mice.Cyclic analogues of α-conotoxin Vc1.1 inhibit colonic nociceptors and provide analgesia in a mouse model of chronic abdominal pain.Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception.Contribution of membrane receptor signalling to chronic visceral pain.Chronic linaclotide treatment reduces colitis-induced neuroplasticity and reverses persistent bladder dysfunctionVisceral PainTetrodotoxin-sensitive voltage-gated sodium channels regulate bladder afferent responses to distensionMechanisms Underlying Overactive Bladder and Interstitial Cystitis/Painful Bladder SyndromeNaV1.1 inhibition can reduce visceral hypersensitivityActivation of pruritogenic TGR5, MrgprA3, and MrgprC11 on colon-innervating afferents induces visceral hypersensitivityTranslating peripheral bladder afferent mechanosensitivity to neuronal activation within the lumbosacral spinal cord of miceLinaclotide treatment reduces endometriosis-associated vaginal hyperalgesia and mechanical allodynia through viscerovisceral cross-talkColonic afferent input and dorsal horn neuron activation differs between the thoracolumbar and lumbosacral spinal cordInnate immune response to bacterial urinary tract infection sensitises high-threshold bladder afferents and recruits silent nociceptors
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description
investigador
@es
researcher
@en
wetenschapper
@nl
name
Luke Grundy
@en
Luke Grundy
@nl
type
label
Luke Grundy
@en
Luke Grundy
@nl
prefLabel
Luke Grundy
@en
Luke Grundy
@nl
P108
P31
P496
0000-0002-3900-7141