References

Ferraz LS, Watashi CM, Colturato-Kido C, Pelegrino MT, Paredes-Gamero EJ, Weller RB, Seabra AB, Rodrigues T (2018) Antitumor Potential of S-Nitrosothiol-Containing Polymeric Nanoparticles against Melanoma. Mol Pharm 15(3):1160-1168. doi: 10.1021/acs.molpharmaceut.7b01001 PMID: 29378125

Objective: To investigate the molecular mechanisms underlying chitosan nanoparticles containing S-nitrosomercaptosuccinic acid (S-nitroso-MSA-CS) induced cytotoxicity in melanoma cells.

Summary: Melanoma cells were more sensitive to cell death than normal melanocytes. S-Nitroso-MSA-CS-induced cytotoxicity exhibited features of caspase-dependent apoptosis, and it was associated with oxidative stress, characterized by increased mitochondrial superoxide production and oxidation of protein thiol groups.

Usage: Immunostaining (1:200)

Related Products: NO-L-Cysteine Mouse Monoclonal, Conjugated (Cat. #AB-T125)

Strichartz G, Khasabov S, Barr T, Wang J, Simone D (2018) Modulation of chronic post-thoracotomy pain by NK-1 neurons in the rostral ventromedial medulla is not paralleled by changes spinal MAPKinase activation. J Pain 19:S14. doi: 10.1016/j.jpain.2017.12.065

Objective: To evaluate SSP-SAP in treatment of tactile hypersensitivity for Chronic Post-Thoractotomy Pain (CPTP).

Summary: SSP-SAP 3 weeks before thoracotomy and rib retraction (TRR) was able to completely prevent CPTP, assayed by tactile hypersensitivity.

Usage: Ablation of Neurokinin-1 receptor (NK-1R)- expressing neurons in the rat rostral ventromedial medulla (RVM), by micro-injection of the specific neurotoxin SSP-SAP.  No effect with treatment of control, Blank-SAP (IT-21).

Related Products: SSP-SAP (Cat. #IT-11), Blank-SAP (Cat. #IT-21)

Ermine CM, Wright JL, Frausin S, Kauhausen JA, Parish CL, Stanic D, Thompson LH (2018) Modelling the dopamine and noradrenergic cell loss that occurs in Parkinson’s disease and the impact on hippocampal neurogenesis. Hippocampus 28(5):327-337. doi: 10.1002/hipo.22835

Objective: The mechanisms underlying reduced neurogenesis in Parkinson’s Disease (PD) are not well established. The authors tested the hypothesis that noradrenergic and dopaminergic depletion, as occurs in PD, impairs hippocampal neurogenesis.

Summary: Mechanisms of neurotransmitter-based regulation of cognition and hippocampal neurogenesis may well overlap under certain conditions but the present results do not suggest a simple relationship associated with the degeneration of the two most prominently affected transmitter systems in PD.

Usage: Rats received 1 mcg Anti-DBH-SAP icv.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Maxwell GK, Szunyogova E, Shorrock HK, Gillingwater TH (2018) Developmental and degenerative cardiac defects in the Taiwanese mouse model of severe spinal muscular atrophy. J Anat 232:965-978. doi: 10.1111/joa.12793 PMID: 29473159

Objective: To investigate changes occurring in the heart, predominantly at pre- and early symptomatic ages, in the Taiwanese mouse model of severe Spinal muscular atrophy (SMA).

Summary: The findings support the requirement to develop systemic therapies for SMA capable of treating non-neuromuscular pathologies.

Usage: Immunohistochemistry, Western blot

Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP)

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)