References

Turnbull MT, Boskovic Z, Coulson EJ (2018) Acute down-regulation of BDNF signaling does not replicate exacerbated amyloid-β levels and cognitive impairment induced by cholinergic basal forebrain lesion. Front Mol Neurosci 11:51. doi: 10.3389/fnmol.2018.00051

Objective: To determine if degeneration of BFCNs causes a decrease in neurotrophin levels in innervated brain areas, which in turn promotes the development of Amyloid beta  pathology and cognitive impairment.

Summary: Lesion of septo-hippocampal BFCNs in a pre-symptomatic transgenic amyloid AD mouse model (APP/PS1 mice) increases soluble Ab levels in the hippocampus, and induces cognitive deficits in a spatial memory task that are not seen in either unlesioned APP/PS1 or non-transgenic littermate control mice. Cognitive decline and Amyloid-beta pathology induced by cholinergic basal forebrain neuron loss occur independent of dysfunctional neuronal BDNF signaling, and may therefore be directly underpinned by reduced cholinergic neurotransmission.

Usage: To lesion BFCNs, a single infusion of murine p75-SAP or control rabbit IgG-SAP (0.4 mg/ml) was stereotaxically injected into the basal forebrain.

Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)

May Z, Kumar R, Fuehrmann T, Tam R, Vulic K, Forero J, Lucas Osma A, Fenrich K, Assinck P, Lee M, Moulson A, Shoichet M, Tetzlaff W, Biernaskie J, Fouad K (2018) Adult skin-derived precursor Schwann cell grafts form growths in the injured spinal cord of Fischer rats. Biomed Mater 13:034101. doi: 10.1088/1748-605X/aa95f8 PMID: 29068322

Objective: To improve grafted cell survival in the injured spinal cord, which is typically low.

Summary: It is of utmost importance to define the precise culture/transplantation parameters for maintenance of normal cell function and safe and effective use of cell therapy.

Usage: Immunohistochemistry (1:500)

Related Products: NGFr (192-IgG, p75) Mouse Monoclonal (Cat. #AB-N43)

Zhuravin IA, Dubrovskaya NM, Tumanova NL, Vasilev DS, Nalivaeva NN (2018) Ontogenetic and phylogenetic approaches for studying the mechanisms of cognitive dysfunctions. Evolutionary Physiology and Biochemistry – Advances and Perspectives: InTech 714-741. doi: 10.5772/intechopen.73666

Summary: The effectiveness of the studies of the pathogenesis of AD and search for the strategies of its prevention and treatment depend on appropriate modeling of the pathological conditions in the brain leading to AD. Traditionally, the main focus on designing animal models of AD was related to the identification of brain areas and mediator systems related to memory. One model employed injections of a monoclonal antibody against growth factor receptor conjugated with saporin (192 IgG-saporin), which also resulted in the loss of cholinergic neurons and cognitive disorder

Related Products: 192-IgG-SAP (Cat. #IT-01)

Jones I, Novikova LN, Novikov LN, Renardy M, Ullrich A, Wiberg M, Carlsson L, Kingham PJ (2018) Regenerative effects of human embryonic stem cell-derived neural crest cells for treatment of peripheral nerve injury. J Tissue Eng Regen Med 12(4):e2099-e2109. doi: 10.1002/term.2642 PMID: 29327452

Objective: To determine if differentiated neural crest cells are promising supporting cell candidates to aid in peripheral nerve repair.

Summary: In this study, neural crest cells were differentiated from human embryonic stem cells. NGFR (mouse monoclonal, 1:100) Immunocytochemistry. The specificity of NGFR antibody was validated by immunocytochemical staining of both hESCs- and MACS-enriched cells.

Related Products: NGFr (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)

Arias-Carrion O, Ortega-Robles E, de Celis-Alonso B, Palasz A, Mendez-Rojas MA, Salas-Pacheco J, Murillo-Rodriguez E (2018) Depletion of hypocretin/orexin neurons increases cell proliferation in the adult subventricular zone. CNS Neurol Disord Drug Targets 17:106-112. doi: 10.2174/1871527317666180314115623

Objective: To establish the relationship between the depletion of orexin neurons and the number of proliferating cells in the subventricular zone.

Summary: The adult subventricular zone is affected by orexinergic signaling, the functional implication of which must be further elucidated.

Usage: 90 ng of Orexin-SAP or pyrogen-free saline was stereotaxically injected into the lateral hypothalamus (3.2 caudal, 1.7 lateral to bregma, 8.1 ventral to the skull surface) of male Wistar rats.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Wang X, Ma S, Wu H, Shen X, Xu S, Guo X, Bolick ML, Wu S, Wang F (2018) Macrophage migration inhibitory factor mediates peripheral nerve injury-induced hypersensitivity by curbing dopaminergic descending inhibition. Exp Mol Med 50(2):e445. doi: 10.1038/emm.2017.271

Objective: To investigate whether the proinflammatory cytokine MIF participates in the regulation of neuropathic hypersensitivity by interacting with and suppressing the descending dopaminergic system.

Summary: MIF functions as a braking factor in curbing dopaminergic descending inhibition in peripheral nerve injury-induced hypersensitivity by mediating Th gene methylation through G9a/SUV39H1-associated H3K9 methylation.

Usage: Anti-DAT-SAP was injected i.t. or i.c.v. with ISO-1 alone or ISO-1 combined with one of the other regulators on Day 7 post-nerve injury for 14 days, and pain behaviors, including 50% withdrawal threshold, mechanical pressure and thermal withdrawal latency, were observed throughout the 70 days post nerve injury.

Related Products: Anti-DAT-SAP (Cat. #IT-25)

Giansanti F, Flavell DJ, Angelucci F, Fabbrini MS, Ippoliti R (2018) Strategies to improve the clinical utility of saporin-based targeted toxins. Toxins (Basel) 10(2):82. doi: 10.3390/toxins10020082

Israel MR, Morgan M, Tay B, Deuis JR (2018) Toxins as tools: Fingerprinting neuronal pharmacology. Neurosci Lett 679:4-14. doi: 10.1016/j.neulet.2018.02.001

Summary: This review article provides an overview of the experimental techniques used to assess the effects that toxins have on neuronal function, as well as discussion on toxins that have been used as tools, with a focus on toxins that target voltage-gated and ligand-gated ion channels.

Related Products: IB4-SAP (Cat. #IT-10), NPY-SAP (Cat. #IT-28)

Kusano-Arai O, Iwanari H, Kudo S, Kikuchi C, Yui A, Akiba H, Matsusaka K, Kaneda A, Fukayama M, Tsumoto K, Hamakubo T (2018) Synergistic cytotoxic effect on gastric cancer cells of an immunotoxin cocktail in which antibodies recognize different epitopes on CDH17. Monoclon Antib Immunodiagn Immunother 37:1-11. doi: 10.1089/mab.2017.0043

Objective: To determine if an immunotoxin cocktail targeted to multiple epitopes has synergistic effects on low expression level cells, which would expand the applicable range of immunotoxin therapy for cancer.

Summary: The combination of immunotoxins with different mechanisms of action in an antibody cocktail will increase cytotoxic activities and decrease side effects.

Usage: The authors applied a monoclonal antibody (mAb) cocktail for one target protein with multiple epitopes. They generated anti-CDH17 mAbs recognizing different epitopes on CDH17 (Cadherin-17). CDH17 is expressed in gastric cancer, hepatocellular carcinoma, colorectal cancer, and pancreatic cancer and has limited distribution in normal tissues. For preparation of 3 immunotoxins, Streptavidin-ZAP was mixed with biotinylated mAbs in equimolar concentrations for 30 minutes at room temperature. The study provides data to demonstrate that the cocktail of different epitope-recognizing immunotoxins has synergistic cytotoxic effects on CDH17-expressing cells.

Related Products: Streptavidin-ZAP (Cat. #IT-27)

Araldi D, Khomula EV, Ferrari LF, Levine JD (2018) Fentanyl induces rapid onset hyperalgesic priming: Type I at peripheral and type II at central nociceptor terminals. J Neurosci 38(9):2226-2245. doi: 10.1523/JNEUROSCI.3476-17.2018

Objective: To evaluate priming, at both nociceptor terminals, the effect of local administration of agents that reverse type I (protein translation) or type II [combination of Src and mitogen-activated protein kinase (MAPK)] priming

Summary: Fentanyl, acting at the -opioid receptor (MOR), induces hyperalgesia and hyperalgesic priming at both the central and peripheral terminal of nociceptors and this is mediated by endoplasmic reticulum Ca2 signaling. Priming in the central terminal is type II, whereas that in the peripheral terminal is type I. Our findings may provide useful information for the design of drugs with improved therapeutic profiles, selectively disrupting individual MOR signaling pathways, to maintain an adequate long-lasting control of pain.

Usage: IB4-SAP was diluted in saline and a dose of 3.2 μg in a volume of 20 μl and administered intrathecally 14 d before experiments

Related Products: IB4-SAP (Cat. #IT-10)