Spinal cord stimulation modulates supraspinal centers of the descending antinociceptive system in rats with unilateral spinal nerve injury
Conclusions:
The serotonergic and noradrenergic pathways of the DAS are involved in the antinociceptive effect of SCS, but activation of the DRN might primarily be responsible for this effect, and the LC may have a smaller contribution. SCS does not potentiate the synthetic enzymes of 5HT and norepinephrine in the neuropathic spinal cord. (Source: Molecular Pain)
Source: Molecular Pain - June 24, 2015 Category: Molecular Biology Authors: Toshiharu TazawaYoshinori KamiyaAyako KobayashiKensuke SaekiMasahito TakiguchiYusuke NakahashiHironobu ShinboriKengo FunakoshiTakahisa Goto Source Type: research
PI3K mediated activation of GSK-3β reduces at-level primary afferent growth responses associated with excitotoxic spinal cord injury dysesthesias
Conclusions:
QUIS induced SCI resulted in inhibition of GSK-3β in primary afferents and enhanced at-level DRG intrinsic growth (neurite elongation and initiation). Early PI3K mediated activation of GSK-3β attenuated QUIS-induced DRG neurite outgrowth and prevented the development of at-level dysesthesias. (Source: Molecular Pain)
Source: Molecular Pain - June 21, 2015 Category: Molecular Biology Authors: Sonja BareissElizabeth DuganKori Brewer Source Type: research
Tolerance to the antinociceptive effects of chronic morphine requires c-Jun N-terminal kinase
Conclusions:
These results demonstrate that JNK signaling plays a crucial role in mediating antinociception as well as chronic tolerance to the antinociceptive effects of morphine in acute, inflammatory, and neuropathic pain states. Thus, inhibition of JNK signaling pathway, via SP600125, represents an efficacious pharmacological approach to delay tolerance to the antinociceptive effects of chronic morphine in diverse pain models. (Source: Molecular Pain)
Source: Molecular Pain - June 12, 2015 Category: Molecular Biology Authors: David MarcusMichael ZeeAlex HughesMatthew YuillAndrea HohmannKen MackieJosée GuindonDaniel Morgan Source Type: research
The opioid peptide dynorphin A induces leukocyte responses via integrin Mac-1 (α M β 2 , CD11b/CD18)
Conclusions:
Together, the results identify dynorphins A and B as novel ligands for Mac-1 and suggest a role for the Dynorphin A-Mac-1 interactions in the induction of nonopiod receptor-dependent effects in leukocytes. (Source: Molecular Pain)
Source: Molecular Pain - June 3, 2015 Category: Molecular Biology Authors: Nataly PodolnikovaJulie BrothwellTatiana Ugarova Source Type: research
The opioid peptide dynorphin A induces leukocyte responses via integrin Mac-1 (αMβ2, CD11b/CD18)
Conclusions:
Together, the results identify dynorphins A and B as novel ligands for Mac-1 and suggest a role for the Dynorphin A-Mac-1 interactions in the induction of nonopiod receptor-dependent effects in leukocytes. (Source: Molecular Pain)
Source: Molecular Pain - June 3, 2015 Category: Molecular Biology Authors: Nataly PodolnikovaJulie BrothwellTatiana Ugarova Source Type: research
MTOR, a New potential target for chronic pain and Opioid-induced tolerance and hyperalgesia
Chronic pain is a major public health problem with limited treatment options. Opioids remain a routine treatment for chronic pain, but extended exposure to opioid therapy can produce opioid tolerance and hyperalgesia. Although the mechanisms underlying chronic pain, opioid-induced tolerance, and opioid-induced hyperalgesia remain to be uncovered, mammalian target of rapamycin (mTOR) is involved in these disorders. The mTOR complex 1 and its triggered protein translation are required for the initiation and maintenance of chronic pain (including cancer pain) and opioid-induced tolerance/hyperalgesia. Given that mTOR inhibito...
Source: Molecular Pain - May 30, 2015 Category: Molecular Biology Authors: Brianna LutzSam NiaMing XiongYuan-Xiang TaoAlex Bekker Source Type: research
Novel expression pattern of neuropeptide Y immunoreactivity in the peripheral nervous system in a rat model of neuropathic pain
Conclusions:
This is the first study to provide a comprehensive description of changes in NPY expression in the periphery after nerve injury. Novel expression of NPY in the skin comes mostly from sprouted sympathetic fibers. This information is fundamental in order to understand where endogenous NPY is expressed, and how it might be acting to modulate pain in the periphery. (Source: Molecular Pain)
Source: Molecular Pain - May 27, 2015 Category: Molecular Biology Authors: Claire MagnussenShih-Ping HungAlfredo Ribeiro-da-Silva Source Type: research
Released lipids regulate Transient Receptor Potential Channel (TRP)-dependent oral cancer pain
Conclusions:
These data reveal a novel mechanism for cancer pain and provide strong direction for future studies evaluating the cellular mechanism regulating the TRP-active lipids by OSCC tumors. (Source: Molecular Pain)
Source: Molecular Pain - May 26, 2015 Category: Molecular Biology Authors: Shivani RuparelMichelle BendeleAshley WallaceDustin Green Source Type: research
Upregulation of T-type Ca2+ channels in long-term diabetes determines increased excitability of a specific type of capsaicin-insensitive DRG neurons
Conclusions:
Capsaicin-insensitive low-pH-sensitive type of DRG neurons shows diabetes-induced upregulation of Cav3.2 subtype of T-type channels. This upregulation results in the increased excitability of these neurons and may contribute to nonthermal nociception at a later-stage diabetes. (Source: Molecular Pain)
Source: Molecular Pain - May 20, 2015 Category: Molecular Biology Authors: Dmytro DuzhyyViacheslav Viatchenko-KarpinskiEugen KhomulaNana VoitenkoPavel Belan Source Type: research
Pain perception in acute model mice of Parkinson’s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
Conclusions:
These results suggest that the dopaminergic nigrostriatal pathway may have a role in inhibiting noxious stimuli, and that abnormal inflammatory responses and neural activity in basal ganglia is correlated to pain processing in PD induced by MPTP treatment. (Source: Molecular Pain)
Source: Molecular Pain - May 17, 2015 Category: Molecular Biology Authors: Jihye ParkChae-Seok LimHyunhyo SeoChung-Ah ParkMin ZhuoBong-Kiun KaangKyungmin Lee Source Type: research
Sodium channel NaV1.7 in vascular myocytes, endothelium, and innervating axons in human skin
Conclusions:
These observations suggest that the activity of mutant Nav1.7 channels in smooth muscle cells of skin vasculature and innervating sensory and sympathetic fibers contribute to the skin reddening and/or pain in IEM and PEPD. (Source: Molecular Pain)
Source: Molecular Pain - May 9, 2015 Category: Molecular Biology Authors: Frank RicePhillip AlbrechtJames WymerJoel BlackIngemar MerkiesCatharina FaberStephen Waxman Source Type: research
Polysulfide evokes acute pain through the activation of nociceptive TRPA1 in mouse sensory neurons
Conclusions:
The present data suggest that polysulfide functions as pronociceptive substance through the activation of TRPA1 in sensory neurons. Since the potency of polysulfide is higher than parental H2S and this sulfur compound is generated under pathophysiological conditions, it is suggested that polysulfide acts as endogenous ligand for TRPA1. Therefore, TRPA1 may be a promising therapeutic target for endogenous sulfur compound-related algesic action. (Source: Molecular Pain)
Source: Molecular Pain - May 2, 2015 Category: Molecular Biology Authors: Yukari HatakeyamaKenji TakahashiMakoto TominagaHideo KimuraToshio Ohta Source Type: research
Minocycline does not affect long-term potentiation in the anterior cingulate cortex of normal adult mice
It has been reported that activated microglia plays important roles in chronic pain-related sensory signaling at the spinal cord dorsal horn. Less is known about the possible contribution of microglia to cortical plasticity that has been found to be important for chronic pain. In the present study, we used a 64-channel multi-electrode array recording system to investigate the role of microglia in cortical plasticity of the anterior cingulate cortex (ACC) in normal adult mice. We found that bath application of minocycline, an inhibitor of microglial activation, had no effect on postsynaptic LTP (post-LTP) induced by theta b...
Source: Molecular Pain - May 2, 2015 Category: Molecular Biology Authors: Qian SongMing-Gang LiuMin Zhuo Source Type: research
In vivo patch-clamp analysis of the antinociceptive actions of TRPA1 activation in the spinal dorsal horn
Conclusions:
TRPA1 appears to be localized not only at presynaptic terminals on SG neurons, enhancing glutamate release, but also in the terminals of primary afferents innervating spinal inhibitory interneurons, which have synaptic interactions with SG neurons. This study offers further insight into the mechanisms underlying the possible antinociceptive actions of TRPA1 activation in the spinal dorsal horn. Our findings suggest that pharmacological activation of spinal TRPA1 channels may have therapeutic potential for the treatment of pain. (Source: Molecular Pain)
Source: Molecular Pain - April 21, 2015 Category: Molecular Biology Authors: Manabu YamanakaWataru TaniguchiNaoko NishioHiroshi HashizumeHiroshi YamadaMunehito YoshidaTerumasa Nakatsuka Source Type: research
Chronic dry eye symptoms after LASIK: parallels and lessons to be learned from other persistent post-operative pain disorders
Laser in-situ keratomileusis (LASIK) is a commonly performed surgical procedure used to correct refractive error. LASIK surgery involves cutting a corneal flap and ablating the stroma underneath, with known damage to corneal nerves. Despite this, the epidemiology of persistent pain and other long-term outcomes after LASIK surgery are not well understood. Available data suggest that approximately 20-55% of patients report persistent eye symptoms (generally regarded as at least 6 months post-operation) after LASIK surgery. While it was initially believed that these symptoms were caused by ocular surface dryness, and referre...
Source: Molecular Pain - April 21, 2015 Category: Molecular Biology Authors: Alexandra LevittAnat GalorJayne WeissElizabeth FelixEden MartinDennis PatinKonstantinos SarantopoulosRoy Levitt Source Type: research
