Reduced antinociception and plasma extravasation in mice lacking a neuropeptide Y receptor
It is concluded that the Y1 receptor is required for central physiological and pharmacological NPY-induced analgesia and that its activation is both sufficient and required for the release of substance P and initiation of neurogenic inflammation.
Effect of low- and high-frequency TENS on Met-enkephalin-Arg-Phe and dynorphin A immunoreactivity in human lumbar CSF
Local corticosteroid application blocks transmission in normal nociceptive C‐fibres
The corticosteroid was found to suppress the transmission in thin unmyelinated C‐fibres but not in myelinated A‐beta fibres, which suggests a direct membrane action.
Nociceptin or antinociceptin: potent spinal antinociceptive effect of orphanin FQ/nociceptin in the rat.
It is reported that intrathecal orphanin FQ produces dose-dependent depression of a spinal nociceptive flexor reflex in the rat and agonists of its receptor may represent novel analgesics for pain conditions which are not responsive to existing pharmacological therapy.
Essential role of Ret for defining non‐peptidergic nociceptor phenotypes and functions in the adult mouse
The results show that Ret is critical for expression of several molecular substrates participating in the detection and transduction of sensory stimuli, resulting in altered physiology following Ret deficiency, and proposes that elevated pain responses could be contributed by GPR35, which is dysregulated in adult Ret‐deficient mice.
Decreased GABA immunoreactivity in spinal cord dorsal horn neurons after transient spinal cord ischemia in the rat
Increased nociceptive response in mice lacking the adenosine A1 receptor
Hyperalgesia and increased neuropathic pain-like response in mice lacking galanin receptor 1 receptors
Central inhibitory dysfunctions: Mechanisms and clinical implications
- Z. Wiesenfeld‐Hallin, H. Aldskogius, G. Grant, J. Hao, T. Hökfelt, X. J. Xu
- Biology, PsychologyBehavioral and Brain Sciences
- 1 September 1997
Dysfunction of central inhibition involving GABA and endogenous opioids may be a factor underlying the development of sensory abnormalities and/or pain following injury to neural tissue.