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Neuromuscular plasticity in a mouse neurotoxic model of spinal motoneuronal loss.
Gulino R, Vicario N, Giunta MAS, Spoto G, Calabrese G, Vecchio M, Gulisano M, Leanza G, Parenti R (2019) Neuromuscular plasticity in a mouse neurotoxic model of spinal motoneuronal loss. Int J Mol Sci 20(6):1500. doi: 10.3390/ijms20061500
Objective: To use a neurotoxic model of spinal motoneuron depletion, induced by injection of CTB-SAP, to investigate the possible occurrence of compensatory changes in both the muscle and spinal cord.
Summary: Plastic changes in surviving motoneurons produce a functional restoration probably similar to the compensatory changes occurring in disease. These changes could be driven by glutamatergic signaling; astrocytes contacting surviving motoneurons may support this process.
Usage: Mice received 2 injections of CTB-SAP (3 mcg CTB-Sap in 2 mcL PBS) into the medial and lateral left gastrocnemius muscle.
Related Products: CTB-SAP (Cat. #IT-14)
Waterpipe smoke effect on oxidative stress levels in buccal cells using MAWI i-SWAB tubes
Mouawad J, Azar JA, Bassil M (2019) Waterpipe smoke effect on oxidative stress levels in buccal cells using MAWI i-SWAB tubes. Biomark J 5(1):1-6. doi: 10.36648/2472-1646.5.1.57 PMID: 909090
Objective: To evaluate the effect of water pipe smoke on oxidative stress levels in buccal cells, using MAWI i-SWAB tubes for the detection of different protein oxidation biomarkers (S-glutathionylation, S-nitrosylation and tyrosine nitration). Furthermore, these tubes were used for the revelation of iNOS and NOX2.
Summary: Results confirmed the findings about the ability of these tubes to detect S-nitrosylation, nitrotyrosine, as well as S-glutathionylation. Results showed also the presence of immature NOX2 in human buccal cells equally.
Usage: Western blot
Related Products: NO-L-Cysteine Mouse Monoclonal, Conjugated (Cat. #AB-T125)
Inflammatory mediators of opioid tolerance: Implications for dependency and addiction.
Eidson LN, Murphy AZ (2019) Inflammatory mediators of opioid tolerance: Implications for dependency and addiction. Peptides 115:51-58. doi: 10.1016/j.peptides.2019.01.003
Objective: To determine what mediates opioid tolerance and alterations in glutamate homeostasis.
Summary: Site-specific lesions of PAG MOR-containing neurons using Dermorphin-SAP significantly reduce the antinociceptive effects of systemic morphine suggesting that PAG MOR is critical for morphine action.
Usage: Rats were injected with 3 pmol of Dermorphin-SAP (Cat. #IT-12) into the PAG. Blank-SAP (Cat. #IT-21) was used as a control.
Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Blank-SAP (Cat. #IT-21)
Kangxianling decoction prevents renal fibrosis in rats with 5/6 nephrectomy and inhibits Ang II-induced ECM production in glomerular mesangial cells.
Ji J, Tao P, He L (2019) Kangxianling decoction prevents renal fibrosis in rats with 5/6 nephrectomy and inhibits Ang II-induced ECM production in glomerular mesangial cells. J Pharmacol Sci 139(4):367-372. doi: 10.1016/j.jphs.2019.03.003 PMID: 30929858
Objective: To investigate effects of Kangxianling decoction on renal fibrosis in a rat model of 5/6 Nephrectomy (5/6 N) in vivo and in angiotensin II (Ang II)-treated rat glomerular mesangial cells (HBZY-1) in vitro.
Summary: Kangxianling decoction could reduce renal fibrosis, accompanied by inhibiting the production of ECM proteins and JNK, along with downregulation of TGF-β, Ang II.
Usage: Western blot analysis (1:100).
Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP)
Knockdown of fidgetin improves regeneration of injured axons by a microtubule-based mechanism.
Matamoros AJ, Tom VJ, Wu D, Rao Y, Sharp DJ, Baas PW (2019) Knockdown of fidgetin improves regeneration of injured axons by a microtubule-based mechanism. J Neurosci 39(11):2011-2024. doi: 10.1523/JNEUROSCI.1888-18.2018 PMID: 30647150
Objective: To test whether fidgetin knockdown assists axonal regeneration.
Summary: Results show that DRG neurons in which fidgetin was knocked down displayed enhanced regeneration of axons across the dorsal root entry zone into the spinal cord. The results establish fidgetin as a novel therapeutic target to augment nerve regeneration.
Usage: immunohistochemistry
Related Products: NGFr (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)
Serotonin and motherhood: From molecules to mood.
Pawluski JL, Li M, Lonstein JS (2019) Serotonin and motherhood: From molecules to mood. Front Neuroendocrinol 53:100742. doi: 10.1016/j.yfrne.2019.03.001
Summary: Serotonin may affect how mothers perceive or behaviorally readjust to changes in the sensory cues emitted by their offspring as they age. The DR serotonin-lesioned mothers studied by Holschbach and colleagues (2018) were much less maternally aggressive, which was concomitant with reduced serotonin-immunoreactive fiber density in the anterior hypothalamus, a brain site previously implicated in serotonin’s influence on aggressive behaviors in male animals.
Related Products: Anti-SERT-SAP (Cat. #IT-23)
Inhibition of methamphetamine self-administration and reinstatement by central blockade of angiotensin II receptor in rats.
Xu X, Pan J, Li X, Cui Y, Mao Z, Wu B, Xu H, Zhou W, Liu Y (2019) Inhibition of methamphetamine self-administration and reinstatement by central blockade of angiotensin II receptor in rats. J Pharmacol Exp Ther 369(2):244-258. doi: 10.1124/jpet.118.255729 PMID: 30867225
Objective: To explore the role of central angiotensin II receptor (ATR) in drug taking and seeking behavior associated with methamphetamine (METH) use disorder.
Summary: The AT1R-PLCβ-CREB signaling pathway was found to be associated with the effect of AT1R on the drug-taking and drug-seeking behavior involving METH use disorder.
Usage: Membranes were incubated at 4°C overnight (1:1000). Western blot.
Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP)
Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats
Dobryakova YV, Volobueva MN, Manolova AO, Medvedeva TM, Kvichansky AA, Gulyaeva NV, Markevich VA, Stepanichev MY, Bolshakov AP (2019) Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats. Front Neurosci 13:146. doi: 10.3389/fnins.2019.00146
Objective: To study the histopathology of the hippocampus and the responses of microglia and astrocytes using immunohistochemistry and neuroglial gene expression.
Summary: Cholinergic degeneration in the medial septal area induced by intracerebroventricular administration of 192IgG-saporin results in an increase in the number of microglial cells and neuron degeneration in the dorsal hippocampus.
Usage: 192-IgG-SAP was injected bilaterally into both ventricles (i.c.v.) at a dose of 4 μg/site.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target.
Bahari Z, Meftahi GH (2019) Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target. Br J Pharmacol 176(14):2366-2381. doi: 10.1111/bph.14580
Objective: To provide an an overview of the cellular mechanisms through which brainstem adrenergic descending inhibitory processing can alter spinal pain transmission to the higher centres, and how these pathways change in neuropathic pain conditions focusing on the role of spinal α2‐adrenoceptors in the spinal dorsal horn.
Summary: The α2‐adrenoceptor agonist may be useful to treat neuropathic pain.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
Noradrenergic terminals are the primary source of α2-adrenoceptor mediated dopamine release in the medial prefrontal cortex.
Devoto P, Flore G, Saba P, Scheggi S, Mulas G, Gambarana C, Spiga S, Gessa GL (2019) Noradrenergic terminals are the primary source of α2-adrenoceptor mediated dopamine release in the medial prefrontal cortex. Prog Neuropsychopharmacol Biol Psychiatry 90:97-103. doi: 10.1016/j.pnpbp.2018.11.015
Objective: To clarify the relative contribution of dopamine (DA) release from noradrenergic and dopaminergic terminals to DA output induced by blockade of α2-adrenoreceptors and the norepinephrine transporter.
Related Products: Anti-DBH-SAP (Cat. #IT-03)