HCN2 ion channels play a central role in inflammatory and neuropathic pain
The rate of action potential firing in nociceptors is a major determinant of the intensity of
pain. Possible modulators of action potential firing include the HCN ion channels, which …
pain. Possible modulators of action potential firing include the HCN ion channels, which …
The cell and molecular basis of mechanical, cold, and inflammatory pain
B Abrahamsen, J Zhao, CO Asante, CM Cendan… - Science, 2008 - science.org
Peripheral pain pathways are activated by a range of stimuli. We used diphtheria toxin to kill
all mouse postmitotic sensory neurons expressing the sodium channel Nav1. 8. Mice …
all mouse postmitotic sensory neurons expressing the sodium channel Nav1. 8. Mice …
HCN2 ion channels: an emerging role as the pacemakers of pain
EC Emery, GT Young, PA McNaughton - Trends in pharmacological …, 2012 - cell.com
Acute nociceptive pain is caused by the direct action of a noxious stimulus on pain-sensitive
nerve endings, whereas inflammatory pain (both acute and chronic) arises from the actions …
nerve endings, whereas inflammatory pain (both acute and chronic) arises from the actions …
Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia
H Ikeda, B Heinke, R Ruscheweyh, J Sandkuhler - Science, 2003 - science.org
Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced
sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the …
sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the …
Impaired nociception and pain sensation in mice lacking the capsaicin receptor
MJ Caterina, A Leffler, AB Malmberg, WJ Martin… - science, 2000 - science.org
The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory
neurons of the “pain” pathway. Heterologously expressed VR1 can be activated by vanilloid …
neurons of the “pain” pathway. Heterologously expressed VR1 can be activated by vanilloid …
Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures
K Zimmermann, A Leffler, A Babes, CM Cendan… - Nature, 2007 - nature.com
Sensory acuity and motor dexterity deteriorate when human limbs cool down, but pain
perception persists and cold-induced pain can become excruciating. Evolutionary pressure …
perception persists and cold-induced pain can become excruciating. Evolutionary pressure …
Neuronal hyperpolarization-activated pacemaker channels drive neuropathic pain
Neuropathic pain is a common and often incapacitating clinical problem for which little
useful therapy is presently available. Painful peripheral neuropathies can have many …
useful therapy is presently available. Painful peripheral neuropathies can have many …
Preserved acute pain and reduced neuropathic pain in mice lacking PKCγ
AB Malmberg, C Chen, S Tonegawa, AI Basbaum - Science, 1997 - science.org
In normal animals, peripheral nerve injury produces a persistent, neuropathic pain state in
which pain is exaggerated and can be produced by nonpainful stimuli. Here, mice that lack …
which pain is exaggerated and can be produced by nonpainful stimuli. Here, mice that lack …
Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy
A Bierhaus, T Fleming, S Stoyanov, A Leffler… - Nature medicine, 2012 - nature.com
This study establishes a mechanism for metabolic hyperalgesia based on the glycolytic
metabolite methylglyoxal. We found that concentrations of plasma methylglyoxal above 600 …
metabolite methylglyoxal. We found that concentrations of plasma methylglyoxal above 600 …
Potent analgesic effects of GDNF in neuropathic pain states
TJ Boucher, K Okuse, DLH Bennett, JB Munson… - Science, 2000 - science.org
Neuropathic pain arises as a debilitating consequence of nerve injury. The etiology of such
pain is poorly understood, and existing treatment is largely ineffective. We demonstrate here …
pain is poorly understood, and existing treatment is largely ineffective. We demonstrate here …