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Distinct roles of NMB and GRP in itch transmission.
Wan L, Jin H, Liu X, Jeffry J, Barry D, Shen K, Peng J, Liu X, Jin J, Sun Y, Kim R, Meng Q, Mo P, Yin J, Tao A, Bardoni R, Chen Z (2017) Distinct roles of NMB and GRP in itch transmission. Sci Rep 7:15466.. doi: 10.1038/s41598-017-15756-0
Summary: To examine the role of NMBR+ dorsal horn neurons in itch and pain transmission, the authors treated mice with NMB-SAP (Cat. #IT-70; 2–3 μg, i.t.) at which no side effects were observed. NMB-SAP treated mice barely showed scratching behaviors, whereas control mice exhibited NMB-induced scratching with a rapid onset of scratching responses. These data demonstrate an important role of NMBR+ neurons in itch transmission. In contrast to notable deficits in itch transmission, NMB-SAP treated mice exhibited normal behavioral responses to acute mechanical stimuli, thermal stimuli and tail immersion. The authors also examined inflammatory pain behaviors of NMB-SAP treated mice and found normal nocifensive behaviors.
Related Products: NMB-SAP (Cat. #IT-70)
T-cell mediation of pregnancy analgesia affecting chronic pain in mice.
Rosen S, Ham B, Drouin S, Boachie N, Chabot-Dore A, Austin J, Diatchenko L, Mogil J (2017) T-cell mediation of pregnancy analgesia affecting chronic pain in mice. J Neurosci 37:9819-9827.. doi: 10.1523/JNEUROSCI.2053-17.2017
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
Spinal microglia are required for long-term maintenance of neuropathic pain
Echeverry S, Shi XQ, Yang M, Huang H, Wu Y, Lorenzo L-E, Perez-Sanchez J, Bonin RP, De Koninck Y, Zhang J (2017) Spinal microglia are required for long-term maintenance of neuropathic pain. Pain 158:1792-1801.. doi: 10.1097/j.pain.0000000000000982
Summary: Selective depletion of spinal microglia in male rats with the targeted immunotoxin Mac-1-SAP and blockade of brain derived neurotrophic factor–TrkB signalling with intrathecal TrkB Fc chimera, but not cytokine inhibition, almost completely reversed pain hypersensitivity. To selectively deplete microglia in the spinal cord, Mac-1-SAP was injected intrathecally. In each group, rats received either an intrathecal injection of 12 mg/7 mL of Mac-1-SAP (n = 6-8) or equal volume of 0.9% saline (n 5 6) or the inactive unconjugated toxin, Saporin (n = 6).)
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06), Saporin (Cat. #PR-01)
Current and future issues in the development of spinal agents for the management of pain.
Yaksh T, Fisher C, Hockman T, Wiese A (2017) Current and future issues in the development of spinal agents for the management of pain. Curr Neuropharmacol 15:232-259.. doi: 10.2174/1570159×14666160307145542
Summary: Although conscious pain experience is driven by signals mediated supraspinally, the more high intensity pain generated by strong stimuli, tissue injury, and nerve injury is encoded at the spinal dorsal horn level. The control of pain signals at the spinal dorsal horn level is a tempting target for targeted pain therapy. This review discusses the potential targets for pain therapeutics in the spinal dorsal horn, and some of the spinal agents used to modulate pain transmission through that location. The use of SSP-SAP (Cat. #IT-11) is mentioned as a neurokinin-1 targeted molecule that can block some pain transmission.
Related Products: SSP-SAP (Cat. #IT-11)
Suppression of asparaginyl endopeptidase attenuates breast cancer-induced bone pain through inhibition of neurotrophin receptors
Yao P, Ding Y, Han Z, Mu Y, Hong T, Zhu Y, Li H (2017) Suppression of asparaginyl endopeptidase attenuates breast cancer-induced bone pain through inhibition of neurotrophin receptors. Mol Pain 13:744806917708127. doi: 10.1177/1744806917708127 PMID: 28554249
Objective: To determine the functions and targeted suppression of asparaginyl endopeptidase (AEP) in a mouse model of breast cancer-induced bone pain.
Summary: Targeted suppression of AEP with specific small compounds significantly reduced bone pain while purified recombinant AEP proteins increased bone pain. AEP aggravates the development of breast cancer bone metastasis and bone pain by increasing the expression of neurotrophin receptors. AEP might be an effective target for treatment of breast cancer-induced bone pain.
Usage: Western blot
Related Products: NGFR (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)
Mediation of movement-induced breakthrough cancer pain by IB4-binding nociceptors in rats.
Havelin J, Imbert I, Sukhtankar D, Remeniuk B, Pelletier I, Gentry J, Okun A, Tiutan T, Porreca F, King T (2017) Mediation of movement-induced breakthrough cancer pain by IB4-binding nociceptors in rats. J Neurosci 37:5111-5122.. doi: 10.1523/JNEUROSCI.1212-16.2017
Objective: To define a novel preclinical measure of movement-induced breakthrough pain (BTP) that is observed in the presence of morphine controlling ongoing pain.
Summary: Novel compounds targeting IB4-binding nociceptors may improve pain management for cancer pain patients and other patient populations suffering from BTP that is inadequately treated by currently available medications.
Usage: To determine the effect of eliminating input from IB4-binding fibers, separate groups of rats received spinal administration of IB4-SAP or the control, Blank-SAP (3.2 mcg/20 mcl saline) followed by a 10 mcl flush of saline. Movement of an air bubble placed between drug solution and saline was used to monitor progress of the injection.
Related Products: IB4-SAP (Cat. #IT-10), Blank-SAP (Cat. #IT-21)
Effect and mechanism of inhibition of PI3K/Akt/mTOR signal pathway on chronic neuropathic pain and spinal microglia in a rat model of chronic constriction injury
Guo JR, Wang H, Jin XJ, Jia DL, Zhou X, Tao Q (2017) Effect and mechanism of inhibition of PI3K/Akt/mTOR signal pathway on chronic neuropathic pain and spinal microglia in a rat model of chronic constriction injury. Oncotarget 8(32):52923-52934. doi: 10.18632/oncotarget.17629 PMID: 28881783
Objective: To explore the effects of inhibition of PI3K/Akt/mTOR signal pathway on chronic neuropathic pain (CNP) and spinal microglia in a rat model of chronic constriction injury (CCI).
Summary: Inhibition of PI3K/Akt/mTOR signal pathway may alleviate CNP and reduce microglia and GFAP and NGF expressions in marrow in a rat model of CCI.
Usage: immunofluorescence assay (1:500)
Related Products: NGFR (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)
Cerebral cholinergic mechanisms in pain: CBF lesions vs systemic scopolamine.
Wiley RG, Yezierski R, Vierck Jr CJ (2016) Cerebral cholinergic mechanisms in pain: CBF lesions vs systemic scopolamine. Neuroscience 2016 Abstracts 525.15 / SS2. Society for Neuroscience, San Diego, CA.
Summary: Cholinergic inputs to the cerebral cortex and limbic system, originating primarily from the cholinergic basal forebrain (CBF), play an important role in cortical sensory processing, largely through modulation of inhibitory interneurons. Cholinergic agonists given spinally, intracerebroventricularly (ICV) or systemically depress reflex nocifensive responses, but systemic cholinergic antagonists also depress some affective responses to pain and impair attention to aversive stimuli and stress reactions. In the present study, we determined the effects of selective cerebral cholinergic denervation, using ICV microinjection of 4 ug of 192-saporin in 10 μl (Advanced Targeting Systems, San Diego, CA) on operant thermal escape responses to aversive thermal stimuli (10° C, 44.5° C) and hyperalgesic effect of sound stress (ten X 30 sec bursts of 100 dB white noise over a 15 min period, 20 mins prior to thermal escape testing) in normal and CBF-lesioned rats compared to effects of systemic cholinergic antagonism (0.1 mg/kg, i.p., scopolamine, 20 minutes prior to thermal escape testing) in intact, normal rats. All rats were on the thermal escape task prior to either scopolamine, or sound stress testing and prior to ICV 192-saporin. At the conclusion of behavioral testing, choline acetyltransferase immunohistochemistry confirmed that 192-sap produced 62-81% loss of CBF cholinergic neurons. CBF-lesioned rats showed decreased thermal escape responses to both temperatures (10°C and 44.5°C) for >19 weeks. There also was no increase in escape responding (hyperalgesia) after sound stress as seen in normal rats. Scopolamine in normal rats produced decreased thermal escape responses to cold (2° C, 6°C and 10° C) and to heat (44.5° C). These results suggest that systemic scopolamine mimics the effects of CBF destruction on pain and together the overall results are interpreted to indicate an important role for the CBF in cerebral pain processing. These findings may be relevant to clinical pain care in patients with cerebral cholinergic dysfunction, such as Alzheimer’s disease.
Related Products: 192-IgG-SAP (Cat. #IT-01)
GABA-A receptor activity in the noradrenergic locus coeruleus drives trigeminal neuropathic pain in the rat; contribution of NAα1 receptors in the medial prefrontal cortex.
Kaushal R, Taylor B, Jamal A, Zhang L, Ma F, Donahue R, Westlund K (2016) GABA-A receptor activity in the noradrenergic locus coeruleus drives trigeminal neuropathic pain in the rat; contribution of NAα1 receptors in the medial prefrontal cortex. Neuroscience 334:148-159. doi: 10.1016/j.neuroscience.2016.08.005
Summary: The goal of this study was to investigate the role of the locus coeruleus (LC) in a rat orofacial pain model of trigeminal neuropathy induced by chronic constrictive injury of the infraorbital nerve (CCI-ION). Mechanical thresholds to von Frey filaments were tested on whisker pads to evaluate neuropathic pain behavior; pain was indicated by development of mechanical hypersensitivity. Noradrenergic (NA) neurons were lesioned with 5-mcg injections of Anti-DBH-SAP (Cat. #IT-03) into the left lateral ventricle. Mouse-IgG-SAP (Cat. #IT-18) was used as a control. After ablation of NA neurons there was a notable increase in the mechanical threshold compared to control animals. They also targeted coeruleotrigeminal NA neurons by injecting Anti-DBH-SAP into the trigeminal brainstem nuclei bilaterally in one animal and saw similar results. Injecting a GABAA receptor antagonist into the LC after injury had an inhibitory effect on nerve injury induced hypersensitivity. Injection of a NAα1 receptor antagonist, but not a NAα2 receptor antagonist, into the medial prefrontal cortex (mPFC) alleviates mechanical hypersensitivity. They conclude that GABAA-mediated activation of NA neurons during CCI-ION can facilitate hypersensitivity through NAα1 receptors in the mPFC, and that the LC is a chronic pain generator.
Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)
Gi-protein-coupled 5-HT1B/D receptor agonist sumatriptan induces type I hyperalgesic priming.
Araldi D, Ferrari L, Levine J (2016) Gi-protein-coupled 5-HT1B/D receptor agonist sumatriptan induces type I hyperalgesic priming. Pain 157:1773-1782. doi: 10.1097/j.pain.0000000000000581
Summary: The present study explored the possibility that, like MOR and A1-adenosine receptor agonists, triptans would also induce type II hyperalgesic priming. In addition, they explored the 5-HT receptor subtypes at which triptans act (5-HT1B, 5-HT1D and 5-HT7) to induce priming. They report that while sumatriptan, a prototypical 5-HT1B/D receptor agonist induces hyperalgesic priming, this priming meets the criteria for type I rather than type II priming. Isolectin B4 (IB4)-saporin (Cat. #IT-10), was diluted in saline, and a dose of 3.2 μg, in a volume of 20 μL was administered intrathecally to rats. The neurotoxin [Sar9,Met(O2) 11]-substance P-saporin (SSP-Saporin, Cat. #IT-11) was diluted in saline, and a dose of 100 ng, in a volume of 20 μL was administered intrathecally. In a model of pain chronification, sumatriptan induces both mechanical hyperalgesia at the site of injection and type I hyperalgesic priming, in nociceptors innervating the cutaneous injection site.
Related Products: IB4-SAP (Cat. #IT-10), SSP-SAP (Cat. #IT-11)