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Involvement of lysophosphatidic acid-induced astrocyte activation underlying the maintenance of partial sciatic nerve injury-induced neuropathic pain
Ueda H, Neyama H, Nagai J, Matsushita Y, Tsukahara T, Tsukahara R (2018) Involvement of lysophosphatidic acid-induced astrocyte activation underlying the maintenance of partial sciatic nerve injury-induced neuropathic pain. Pain 159:2170-2178. doi: 10.1097/j.pain.0000000000001316
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
Targeting macrophage and microglia activation with colony stimulating factor 1 receptor inhibitor is an effective strategy to treat injury-triggered neuropathic pain
Lee S, Shi XQ, Fan A, West B, Zhang J (2018) Targeting macrophage and microglia activation with colony stimulating factor 1 receptor inhibitor is an effective strategy to treat injury-triggered neuropathic pain. Mol Pain 14:1744806918764979. doi: 10.1177/1744806918764979
Summary: Depletion of spinal microglia with Mac-1-SAP was able to prevent and reverse neuropathic pain behavior.
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
CD44 signaling mediates high molecular weight hyaluronan-induced antihyperalgesia.
Ferrari LF, Khomula EV, Araldi D, Levine JD (2018) CD44 signaling mediates high molecular weight hyaluronan-induced antihyperalgesia. J Neurosci 38(2):308-321. doi: 10.1523/JNEUROSCI.2695-17.2017
Objective: To study the role of the cognate hyaluronan receptor, CD44, signaling in anti-hyperalgesia induced by high molecular weight hyaluronan (HMWH).
Summary: These results demonstrate the central role of CD44 signaling in HMWH-induced anti-hyperalgesia, and establish it as a therapeutic target against inflammatory and neuropathic pain.
Usage: Both IB4-SAP and SSP-SAP were diluted in saline to doses previously shown to deplete nonpeptidergic (3.2 mcg/rat for IB4-SAP) and peptidergic (100 ng/rat for SSP-SAP) fibers. The toxins were administered intrathecally, in a volume of 20 mcl, 14 d before intradermal injection of LMWH on the dorsum of the hindpaw. Treatment with either conjugate, or a combination of the two, did not significantly affect mechanical nociceptive threshold.
Related Products: IB4-SAP (Cat. #IT-10), SSP-SAP (Cat. #IT-11), Anti-CD44-SAP (Cat. #IT-72)
Attenuation of the infiltration of angiotensin ii expressing CD3+ T-cells and the modulation of nerve growth factor in lumbar dorsal root ganglia – a possible mechanism underpinning analgesia produced by EMA300, an Angiotensin II type 2 (AT2) receptor antagonist
Khan N, Muralidharan A, Smith MT (2017) Attenuation of the infiltration of angiotensin ii expressing CD3+ T-cells and the modulation of nerve growth factor in lumbar dorsal root ganglia – a possible mechanism underpinning analgesia produced by EMA300, an Angiotensin II type 2 (AT2) receptor antagonist. Front Mol Neurosci 10:389. doi: 10.3389/fnmol.2017.00389 PMID: 29200998
Objective: To investigate the cellular and molecular mechanism of action of selective small molecule angiotensin II type 2 (AT2) receptor antagonists in the alleviation of peripheral neuropathic pain.
Summary: The analgesic effect of EMA300 in CCI-rats involves multimodal actions that appear to be mediated at least in part by a significant reduction in the otherwise increased expression levels of Ang II as well as the number of Ang II-expressing CD3+ T-cells in the ipsilateral lumbar DRGs of CCI-rats.
Usage: Immunocytochemistry; specifically labeled HEK cells expressing the AT2 but not the AT1 receptor or the non-transfected HEK-cells.
Related Products: Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)
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)
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)
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)
Dynamics of spinal microglia repopulation following an acute depletion.
Yao Y, Echeverry S, Shi X, Yang M, Yang Q, Wang G, Chambon J, Wu Y, Fu K, De Koninck Y, Zhang J (2016) Dynamics of spinal microglia repopulation following an acute depletion. Sci Rep 6:22839. doi: 10.1038/srep22839
Summary: This study confirms that similar to microglia in the brain, spinal microglia can repopulate rapidly following elimination, which is driven essentially by a self-renewal process. To deplete microglia in spinal cords, Mac-1-SAP (Cat. #IT-06) was injected i.t. (7 μl, 1.6 μg/μl) at the level of L4-L5 in mouse. The results support the concept that microglia repopulation, whether in the brain or in the spinal cord, is the consequence of onsite resident microglia proliferation. Newly generated microglia are fully functional and are able to respond to peripheral nerve injury and contribute to the development of neuropathic pain.
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
A small molecule angiotensin II type 2 receptor (AT₂R) antagonist produces analgesia in a rat model of neuropathic pain by inhibition of p38 mitogen-activated protein kinase (MAPK) and p44/p42 MAPK activation in the dorsal root ganglia
Smith MT, Woodruff TM, Wyse BD, Muralidharan A, Walther T (2013) A small molecule angiotensin II type 2 receptor (AT₂R) antagonist produces analgesia in a rat model of neuropathic pain by inhibition of p38 mitogen-activated protein kinase (MAPK) and p44/p42 MAPK activation in the dorsal root ganglia. Pain Med 14(10):1557-1568. doi: 10.1111/pme.12157 PMID: 23742186
Objective: To elucidate the mechanism through which EMA300, a small molecule antagonist of the angiotensin II type 2 receptor (AT2R) with >1,000-fold selectivity over the angiotensin II type 1 receptor, produces analgesia in a rodent model of neuropathic pain.
Summary: Augmented angiotensin II/AT2R signaling in the DRGs of CCI rats is attenuated by EMA300 to block p38 MAPK and p44/p42 MAPK activation, a mechanism with clinical validity for alleviating neuropathic pain.
Usage: Immunostaining (1:250), rat DRG sections
Related Products: Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)
Knockdown of noradrenergic locus coeruleus (LC) neurons alleviates chronic orofacial pain
Kaushal R, Ma F, Zhang L, Bright CR, Taylor BK, Westlund KN (2012) Knockdown of noradrenergic locus coeruleus (LC) neurons alleviates chronic orofacial pain. Neuroscience 2012 Abstracts 164.19. Society for Neuroscience, New Orleans, LA.
Summary: Trigeminal neuralgia (TN) is an excruciating and debilitating form of clinical orofacial pain. Noradrenergic locus coeruleus (LC, pontine A6 neurons) is involved in bidirectional modulation of pain. Multiple studies indicate that LC activity is increased during noxious stimulation and following inflammation or nerve damage. Predominantly known for its role in the feedback inhibition of pain, emerging studies also indicate a contribution of the LC in pain facilitation. For example, lesions of the LC significantly reduce tonic behavioral responses to intraplantar formalin injection, prevent autotomy, and reduce hypersensitivity associated with peripheral nerve injury. In this study we hypothesized that noradrenergic (LC) neurons contribute to the facilitation of chronic pain in TN. We used a rat model of TN involving infraorbital nerve chronic constriction injury (ION-CCI) which produces mechanical hypersensitivity as assessed by a reduction in von Frey threshold. Administration of anti-dopamine-β-hydroxylase saporin (anti-DβH-saporin) toxin was performed for selective elimination of noradrenergic LC neurons or IgG saporin (nonspecific) as the control either by intracerebroventricular (i.c.v space 2) or by bilateral spinal trigeminal nucleus (STN) injections. Under minimal restraint, rats received either no stimulation or repeated stimulation with either a 2 or 15-gm von Frey hair applied directly to the maxillary branch. Withdrawal threshold (tactile allodynia) from von Frey fiber stimulation to the face was not changed as compared to baseline in animals subjected to sham surgery; this was true in both saporin and anti-DβH-saporin groups. However, i.c.v. anti-DβH-saporin significantly increased withdrawal threshold animals with ION-CCI as compared to IgG saporin controls. More selective destruction of the LC-trigeminal pathway with bilateral STN anti-DβH-saporin injection also alleviated behavioral signs of chronic orofacial hyperalgesia. Elimination of noradrenergic LC neurons was confirmed by complete loss of tyrosine hydroxylase (TH) immunoreactivity in anti-DβH-saporin injected animals. Compared to unstimulated controls, mechanical stimulation increased immunoreactive phosphorylated extracellular cell-regulated protein kinase (pERK), a marker of neuronal activity, in the LC and STN. Nerve injury also increased expression of a neuronal injury and stress marker, activating transcription factor 3 (ATF3), in trigeminal ganglia neurons. Together, these results indicate that noradrenergic locus coeruleus neurons facilitate chronic orofacial neuropathic pain.
Related Products: Anti-DBH-SAP (Cat. #IT-03)