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Showing papers in "Neurobiology of Pain in 2019"


Journal ArticleDOI
TL;DR: CRMP2 phosphorylation levels are dysregulated in the SNI model of experimental neuropathy and genetic targeting of CRMP2osphorylation by Cdk5 reverses neuropathic pain.

36 citations


Journal ArticleDOI
TL;DR: Late tPA-induced stable long-lasting CPSP in the mouse model and Therapeutic effects of LPA1 and LPA3 antagonist against the established CPSP are shown.

28 citations


Journal ArticleDOI
TL;DR: Using rat model of neuropathy with multimodal MRI, imaging the reorganization of pain neural circuitry within 8 days of chemotherapy shows loss of anticorrelation between prefrontal cortex and PAG.

28 citations


Journal ArticleDOI
TL;DR: Activation of cAMP-PKA and cGMP-PKG pathways contributes to injury-induced sensory neuron hyperexcitability and PAR2 activation mediates injury- induced cAMP/gMP/cGMP/ PAR2 cAMP dependence on bone cancer pain.

26 citations


Journal ArticleDOI
TL;DR: Narciclasine prevents and reverses paclitaxel-induced mechanical hypersensitivity and hyperalgesic priming in male and female mice.

26 citations


Journal ArticleDOI
TL;DR: The effect of TrkB-Fc on hyperalgesic priming is sexually dimorphic in mice and Microglial BDNF does not contribute to hyperalgeous priming in mice.

23 citations


Journal ArticleDOI
TL;DR: Intradermal injection of cathepsin S induces scratching behaviour in mice and acts as a pruritogen via protease-activated receptor 2(PAR2) in TRPV1-expressing neurons, which can be used as translational model and for testing new indications for cathePSin S inhibitors.

22 citations


Journal ArticleDOI
TL;DR: Voluntary running reduced mechanical and cold allodynia induced by paclitaxel and reduced pac litaxel-induced deficits in hippocampal cellular proliferation in a rodent model of Alzheimer's disease.

21 citations


Journal ArticleDOI
TL;DR: FHF2A and 2B knockdown in DRG neurons leads to gain-of-function in Nav1.7 in an isoform-specific manner, and this results in a cell environment-dependent manner.

16 citations


Journal ArticleDOI
TL;DR: Methanol extract of Cola nitida (MECN) was evaluated for its anti-inflammatory and analgesic activities using rats and mice in this paper, and the results revealed that MECN has both anti inflammatory and pain-causing properties.

15 citations


Journal ArticleDOI
TL;DR: Chronic constriction injury of the infraorbital nerve produced ongoing hyperalgesia and allodynia in this chronic orofacial pain model and a natural history group is essential to disentangle real placebo effects from non-specific analgesic responses.

Journal ArticleDOI
TL;DR: The knock-down of RCP expression the SpVc attenuates mechanical facial allodynia induced by chemical noxious stimulation of the meninges, but have little effect on ongoing pain behaviors in female and male animals.

Journal ArticleDOI
TL;DR: The first awake-rat model of explosive blast-induced traumatic brain injury (blast-TBI) in rats developed ongoing, spontaneous pain and did not result in persistent changes in activity of thalamic or spinal neurons, or in gliosis in these structures.

Journal ArticleDOI
TL;DR: The rat results mirror what has been found in human patients with osteoarthritis, and levels of biochemical mediators differs between ankle and knee injection of MIA in rats.

Journal ArticleDOI
TL;DR: Highlights • Chronic back pain (CBP) showed less positive evaluations of touch and brain-behavior changes in pleasant touch processing may be a marker of pain chronicity.

Journal ArticleDOI
TL;DR: AMPK activators increase P-body formation in DRG neurons in vitro in vitro and treatment with metformin restores normal P- body numbers inDRG neurons from nerve injured mice.

Journal ArticleDOI
TL;DR: The pig PNT model provides better data than rodent for translational pain research and mimics cutaneous human pathologies, unlike rodent.

Journal ArticleDOI
TL;DR: It is explored whether placebo analgesia alters afferent nociceptive processing in healthy adult participants and only placebo responders showed changes in discriminative ability.