Nasal application of neuropeptide S inhibits arthritis pain-related behaviors through an action in the amygdala
In conclusion, nasal application of NPS can inhibit emotional-affective, but not sensory, pain-related behaviors through an action in the amygdala. The beneficial effects of non-invasive NPS application may suggest translational potential. (Source: Molecular Pain)
Source: Molecular Pain - May 29, 2014 Category: Molecular Biology Authors: Georgina MedinaGuangchen JiStéphanie GrégoireVolker Neugebauer Source Type: research
Artemin growth factor increases nicotinic cholinergic receptor subunit expression and activity in nociceptive sensory neurons
Conclusions:
These findings suggest that Artn regulates the expression and composition of nAChRs in GFRalpha3 nociceptors and that these changes contribute to the thermal hypersensitivity that develops in response to Artn injection and perhaps to inflammation. (Source: Molecular Pain)
Source: Molecular Pain - May 22, 2014 Category: Molecular Biology Authors: Kathryn AlbersXiu ZhangCharlotte DigesErica SchwartzCharles YangBrian DavisMichael Gold Source Type: research
Acid mediates a prolonged antinociception via substance P signaling in acid-induced chronic widespread pain
Conclusions:
Acid could mediate a prolonged antinociceptive signaling via the release of substance P from muscle afferent neurons in a non-ASIC3, non-TRPV1 manner. (Source: Molecular Pain)
Source: Molecular Pain - May 21, 2014 Category: Molecular Biology Authors: Wei-Nan ChenChih-Cheng Chen Source Type: research
PAR2-mediated upregulation of BDNF contributes to central sensitization in bone cancer pain
Conclusion:
The present study demonstrated that activation of PAR2 triggered NF-kappaB signaling and significantly upregulated the BDNF function, which critically contributed to the enhancement of glutamatergic transmission in spinal dorsal horn and thermal and mechanical hypersensitivity in the rats with bone cancer. This indicated that PAR2 - NF-kappaB signaling might become a novel target for the treatment of pain in patients with bone cancer. (Source: Molecular Pain)
Source: Molecular Pain - May 5, 2014 Category: Molecular Biology Authors: Yanju BaoWei HouRui LiuYebo GaoXiangying KongLiping YangZhan ShiWeidong LiHonggang ZhengShulong JiangConghuang LiYinggang QinBaojin Hua Source Type: research
Prophylactic cannabinoid administration blocks the development of paclitaxel-induced neuropathic nociception during analgesic treatment and following cessation of drug delivery
Conclusions and implications: Cannabinoids block development of paclitaxel-induced neuropathy and protect against neuropathic allodynia following cessation of drug delivery. Chronic treatment with both mixed CB1/CB2 and CB2 selective cannabinoids increased mRNA expression of cannabinoid receptors (CB1, CB2) in a CB2-dependent fashion. Our results support the therapeutic potential of cannabinoids for suppressing chemotherapy-induced neuropathy in humans. (Source: Molecular Pain)
Source: Molecular Pain - April 18, 2014 Category: Molecular Biology Authors: Elizabeth RahnLiting DengGanesh ThakurKiran VemuriAlexander ZvonokYvonne LaiAlexandros MakriyannisAndrea Hohmann Source Type: research
A simplified up-down method (SUDO) for measuring mechanical nociception in rodents using von Frey filaments
Conclusion:
SUDO thus offers an accurate, fast and user-friendly replacement for the widely used up-down method of Chaplan et al. (Source: Molecular Pain)
Source: Molecular Pain - April 16, 2014 Category: Molecular Biology Authors: Robert BoninCyril BoriesYves De Koninck Source Type: research
The chemerin receptor 23 agonist, chemerin, attenuates monosynaptic C-fibre input to lamina I neurokinin 1 receptor expressing rat spinal cord neurons in inflammatory pain
Conclusions:
These results suggest that the reported ability of ChemR23 agonists to attenuate inflammatory painhypersensitivity may in part be due to a presynaptic inhibition of monosynaptic C-fibre input to laminaI NK1R+ neurons and provides further evidence that ChemR23 represents a promising inflammatorypain target. (Source: Molecular Pain)
Source: Molecular Pain - April 9, 2014 Category: Molecular Biology Authors: Allen DickieCarole Torsney Source Type: research
Retraction: Comparison of central versus peripheral delivery of pregabalin in neuropathic pain states
No description available (Source: Molecular Pain)
Source: Molecular Pain - April 2, 2014 Category: Molecular Biology Authors: Jose MartinezManami KasamatsuAlma Rosales-HernandezLeah HansonWilliam FreyCory Toth Source Type: research
The effect of acupuncture needle combination on central pain processing-an fMRI study
Conclusions:
While both EA2 and EA3 induced a significant degree of deactivation in the human brain regions related to pain processing, the addition of GP stimulation further exerts an inhibitory effect on the ascending spinoreticular pain pathway. Therefore, different needling position as mandated in different empirical acupuncture treatment paradigms may play a different role in modulating pain related neuronal functions. (Source: Molecular Pain)
Source: Molecular Pain - March 25, 2014 Category: Molecular Biology Authors: Albert LeungYi ZhaoShivshil Shukla Source Type: research
Voltage-gated sodium channel expression in mouse DRG after SNI leads to re-evaluation of projections of injured fibers
Conclusions:
The complex regulation of Navs, together with the anatomical rostral shift of the DRG harboring injured fibers in C57BL/6 J mice, help emphasize that caution is necessary and preliminary anatomical experiments should be carried out for gene and protein expression studies after SNI in mouse strains. (Source: Molecular Pain)
Source: Molecular Pain - March 11, 2014 Category: Molecular Biology Authors: Cédric LaedermannMarie PertinMarc SuterIsabelle Decosterd Source Type: research
Correction: shaped magnetic field pulses by multi-coil repetitive transcranial magnetic stimulation (rTMS) differentially modulate anterior cingulate cortex responses and pain in volunteers and fibromyalgia patients
No description available (Source: Molecular Pain)
Source: Molecular Pain - March 4, 2014 Category: Molecular Biology Authors: Alexander TzabazisCarina ApariciMichael RowbothamM SchneiderAmit EtkinDavid Yeomans Source Type: research
Activation of peripheral KCNQ channels attenuates inflammatory pain
Conclusions:
Our findings suggest that the peripheral sensory neuron is the main target for KCNQ channel openers to induce analgesia. Therefore, peripheral KCNQ channel openers that do not penetrate the CNS may be suitable analgesic drugs as they would prevent CNS side effects. (Source: Molecular Pain)
Source: Molecular Pain - February 21, 2014 Category: Molecular Biology Authors: Hiroki HayashiMasashi IwataNoboru TsuchimoriTatsumi Matsumoto Source Type: research
Contribution of anterior cingulate cortex and descending pain inhibitory system to analgesic effect of lemon odor in mice
Conclusions:
These results suggest that the analgesic effect of lemon oil is induced by dopamine-related activation of ACC and the descending pain inhibitory system. (Source: Molecular Pain)
Source: Molecular Pain - February 20, 2014 Category: Molecular Biology Authors: Hiroshi IkedaSyuntaro TakasuKazuyuki Murase Source Type: research
ARA 290, a peptide derived from the tertiary structure of erythropoietin, produces long-term relief of neuropathic pain coupled with suppression of the spinal microglia response
Conclusions:
The erythropoietin-analogue ARA290 dose-dependently reduced allodynia coupled to suppression of the spinal microglia response, suggestive of a mechanistic link between ARA290-induced suppression of central inflammation and relief of neuropathic pain symptoms. (Source: Molecular Pain)
Source: Molecular Pain - February 16, 2014 Category: Molecular Biology Authors: Maarten SwartjesMonique van VelzenMarieke NiestersLeon AartsMichael BrinesAnn DunneAnthony CeramiAlbert Dahan Source Type: research
Toll like receptor (TLR)-4 as a regulator of peripheral endogenous opioid-mediated analgesia in inflammation
Conclusion:
Endogenous opioids from monocytes/macrophages mediate endogenous antinociception in the late phase of inflammation. Peripheral TLR4 stimulation acts as a transient counter-regulatory mechanism for inflammatory pain in vivo, and increases the release of opioid peptides from monocytes in vitro. TLR4 antagonists as new treatments for sepsis and neuropathic pain might unexpectedly transiently enhance pain by impairing peripheral opioid analgesia. (Source: Molecular Pain)
Source: Molecular Pain - February 6, 2014 Category: Molecular Biology Authors: Reine-Solange SauerDagmar HackelLaura MorschelHenrike SahlbachYing WangShaaban MousaNorbert RoewerAlexander BrackHeike Rittner Source Type: research
