Lista de obras -

Activation of pruritogenic TGR5, MrgprA3, and MrgprC11 on colon-innervating afferents induces visceral hypersensitivity

scientific article published on 17 October 2019

Chronic linaclotide treatment reduces colitis-induced neuroplasticity and reverses persistent bladder dysfunction

article

Colonic afferent input and dorsal horn neuron activation differs between the thoracolumbar and lumbosacral spinal cord

artículo científico publicado en 2019

Contribution of membrane receptor signalling to chronic visceral pain.

artículo científico publicado en 2018

Cyclic analogues of α-conotoxin Vc1.1 inhibit colonic nociceptors and provide analgesia in a mouse model of chronic abdominal pain

artículo científico publicado en 2017

Identifying unique subtypes of spinal afferent nerve endings within the urinary bladder of mice

artículo científico publicado en 2017

Innate immune response to bacterial urinary tract infection sensitises high-threshold bladder afferents and recruits silent nociceptors

scientific article published on 01 January 2020

Linaclotide treatment reduces endometriosis-associated vaginal hyperalgesia and mechanical allodynia through viscerovisceral cross-talk

artículo científico publicado en 2019

Mechanisms Underlying Overactive Bladder and Interstitial Cystitis/Painful Bladder Syndrome

artículo científico publicado en 2018

Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.

artículo científico publicado en 2017

NaV1.1 inhibition can reduce visceral hypersensitivity

artículo científico publicado en 2018

Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain

scientific journal article

Tetrodotoxin-sensitive voltage-gated sodium channels regulate bladder afferent responses to distension

article

Translating peripheral bladder afferent mechanosensitivity to neuronal activation within the lumbosacral spinal cord of mice

scientific article published on 01 April 2019

Visceral Pain

scientific article published on 31 October 2018

Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception.

artículo científico publicado en 2018

α-Conotoxin Vc1.1 inhibits human dorsal root ganglion neuroexcitability and mouse colonic nociception via GABAB receptors.

artículo científico publicado en 2016

Lista de obras de

Activation of pruritogenic TGR5, MrgprA3, and MrgprC11 on colon-innervating afferents induces visceral hypersensitivity

Chronic linaclotide treatment reduces colitis-induced neuroplasticity and reverses persistent bladder dysfunction

Colonic afferent input and dorsal horn neuron activation differs between the thoracolumbar and lumbosacral spinal cord

Contribution of membrane receptor signalling to chronic visceral pain.

Cyclic analogues of α-conotoxin Vc1.1 inhibit colonic nociceptors and provide analgesia in a mouse model of chronic abdominal pain

Identifying unique subtypes of spinal afferent nerve endings within the urinary bladder of mice

Innate immune response to bacterial urinary tract infection sensitises high-threshold bladder afferents and recruits silent nociceptors

Linaclotide treatment reduces endometriosis-associated vaginal hyperalgesia and mechanical allodynia through viscerovisceral cross-talk

Mechanisms Underlying Overactive Bladder and Interstitial Cystitis/Painful Bladder Syndrome

Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.

NaV1.1 inhibition can reduce visceral hypersensitivity

Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain

Tetrodotoxin-sensitive voltage-gated sodium channels regulate bladder afferent responses to distension

Translating peripheral bladder afferent mechanosensitivity to neuronal activation within the lumbosacral spinal cord of mice

Visceral Pain

Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception.

α-Conotoxin Vc1.1 inhibits human dorsal root ganglion neuroexcitability and mouse colonic nociception via GABAB receptors.