References

Fujii S, Yoshida S, Inagaki E, Hatou S, Tsubota K, Takahashi M, Shimmura S, Sugita S (2019) Immunological properties of neural crest cells derived from human induced pluripotent stem cells. Stem Cells Dev 28(1):28-43. doi: 10.1089/scd.2018.0058 PMID: 30251915

Objective: To assess the immunological properties of human induced pluripotent stem cells derived neural crest cells (iPSC-NCCs)

Summary: Cultured human NCCs can fully suppress T cell activation in vitro and may be used in cell-based medicine.

Usage: IHC; 1:200 dilution

Related Products: NGFr (ME20.4, p75) Mouse Monoclonal (Cat. #AB-N07)

Qiu M, Li J, Tan L, Zhang M, Zhou G, Zeng T, Li A (2018) Targeted ablation of distal cerebrospinal fluid-contacting nucleus alleviates renal fibrosis in chronic kidney disease. Front Physiol 9:1640. doi: 10.3389/fphys.2018.01640

Objective: To test the hypothesis that distal cerebrospinal fluid-contacting nucleus (dCSF-CNs) might affect the renin-angiotensin system (RAS) in kidney injury progression.

Summary: Less CTB-labeled neurons were found in dCSF-CNs of CTB-SAP-treated rats. Meanwhile, CTB-SAP downregulated AGT, Ang II, AT1R, NOX2, catalase, MCP-1, IL-6, fibronectin, and collagen I, and upregulated ACE2 and Mas receptor. Targeted dCSF-CNs ablation could alleviate renal inflammation and fibrosis in chronic kidney injury.

Usage: CTB-SAP (500 ng) into the lateral ventricles over a 3-min period.

Related Products: CTB-SAP (Cat. #IT-14)

Bailey D, Catron M, Kovtun O, Macdonald R, Zhang Q, Rosenthal S (2018) Single quantum dot tracking reveals serotonin transporter diffusion dynamics are correlated with cholesterol-sensitive threonine 276 phosphorylation status in primary midbrain neurons. ACS Chem Neurosci 9:2534-2541. doi: 10.1021/acschemneuro.8b00214 PMID: 29787674

Objective: Visualizing SERT behavior at the single molecule level in endogenous systems remains a challenge. The authors utilize quantum dot (QD) single particle tracking (SPT) to capture SERT dynamics in primary rat midbrain neurons.

Summary: Results provide new insights into endogenous neuronal SERT mobility and its associations with membrane cholesterol and SERT phosphorylation status.

Usage: Live Cell QD Tracking – Cells were incubated with 5 μg/mL primary SERT antibody in warm fluorescent media at 37 °C and 5% CO2 for 6 min.

Related Products: SERT Mouse Monoclonal (Cat. #AB-N40)

Manzuoerh R, Farahpour MR, Oryan A, Sonboli A (2019) Effectiveness of topical administration of Anethum graveolens essential oil on MRSA-infected wounds. Biomed Pharmacother 109:1650-1658. doi: 10.1016/j.biopha.2018.10.117 PMID: 30551419

Usage: immunohistochemistry (1:500)

Related Products: Fibroblast Growth Factor Rabbit Polyclonal, mammalian (Cat. #AB-07)

Seel S, Eacott M, Langston R, Easton A (2018) Cholinergic input to the hippocampus is not required for a model of episodic memory in the rat, even with multiple consecutive events. Behav Brain Res 354:48-54. doi: 10.1016/j.bbr.2017.06.001

Summary: The authors use 192-IgG-SAP (Cat. #IT-01) to examine episodic memory. Continual trials versions of an episodic memory task are unimpaired by cholinergic lesions of the medial septum. In contrast continual trial versions of a location-context (where-which) task are impaired in the same animals. The results replicate the effects of lesions on one-trial a day versions of the same tasks. Increasing the amount of interference between trials by increasing the overlap of features in consecutive events has no effect on the behavioural outcome of these lesions. The result is interpreted in light of models of acetylcholine function centered around pattern separation.

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

Shibata S, Hayashi R, Okubo T, Kudo Y, Katayama T, Ishikawa Y, Toga J, Yagi E, Honma Y, Quantock AJ, Sekiguchi K, Nishida K (2018) Selective laminin-directed differentiation of human induced pluripotent stem cells into distinct ocular lineages. Cell Rep 25:1668-1679. doi: 10.1016/j.celrep.2018.10.032 PMID: 30404017

Usage: Immunostaining, flow cytometry

Related Products: NGFr (ME20.4, p75) Mouse Monoclonal (Cat. #AB-N07)

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)

Cammarata C, DeRosa ED, Anderson AK (2018) Lifespan and cholinergic changes in cognitive flexibility in rats. Neuroscience 2018 Abstracts 512.05 / GGG8. Society for Neuroscience, San Diego, CA.

Summary: The ability to update one’s mental schemas in order respond flexibly and adaptably – i.e. cognitive flexibility – is crucial to navigating a dynamic environment. Proactive interference (PI) is a phenomenon wherein prior memory impedes the formation of new memories for similar information, biasing behavior toward no-longer-relevant schemas. Thus, overcoming PI is an important aspect of cognitive flexibility. PI is exacerbated during aging, and in turn contributes to age-related deficits in cognitive flexibility. In young animals and young adult humans, resolution of PI has been found to rely on neuromodulatory activity via Acetylcholine (ACh), and ACh levels are known to decline in aging, however it has yet to be demonstrated whether these age-related changes in ACh directly contribute to age-related increase in PI. Here, we first compared PI resolution in middle-aged (13 months, n = 8) and old (23 months, n= 11) male Long Evans rats, finding that old animals were more inefficient in resolving PI when compared to the middle-aged animals. Furthermore we performed cholinergic deafferentation, with the immunotoxin 192-IgG saporin (SAP; 0.2 µl of 0.3 µg/µl dissolved in sterile phosphate buffered sale in each of four locations targeting bilateral anterior and posterior basal forebrain), in our older rats (N= 5 SAP and N=6 Sham) which had no effect on the floor performance of older rats. This suggests that the inability to resolve PI seen in the aged rats may be due to already-depleted levels of ACh. We are currently collecting local field potential data in the prelimbic and posterior parietal cortices in behaving older and younger rats and will combine this with central administration of muscarinic cholinergic pharmacology to continue to examine age-related changes in the cortical dynamics that support cognitive flexibility. Based on prior findings in our laboratory examining similar attentional flexibility, we predict the young animals will demonstrate increased beta band LFP activity in the posterior parietal cortex, and potentially increased beta coherence between prefrontal and posterior parietal cortices, related to successful resolution of PI. We expect such activity to be mitigated by cholinergic antagonists and in the older animals.

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

Daripelli S, Bhayrapuneni G, Tirumalesetty C, Benade V, Subramanian R, Petlu S, Praveena N, Jayarajan P, Shinde A, Badange R, Bhatta V, Nirogi R (2018) SUVN-G3031, H3 receptor inverse agonist produces wake promoting activity in rats with hypocretin-2-saporin lesions of the lateral hypothalamus. Neuroscience 2018 Abstracts 679.23 / VV4. Society for Neuroscience, San Diego, CA.

Summary: Numerous studies have demonstrated that brain histamine plays a crucial role in maintenance of wakefulness, attention, learning and other cognitive processes. SUVN-G3031, a potent H3 receptor inverse agonist is being developed for the treatment of narcolepsy and other sleep related disorders. SUVN-G3031 is one of the lead molecules with hKi of 8.7 nM and has more than 100 fold selectivity against the related GPCRs. SUVN-G3031 exhibited desired pharmacokinetic properties and brain penetration. SUVN-G3031 blocked R-α-methylhistamine induced water intake and increased tele-methylhistamine levels in brain and cerebrospinal fluid. A single oral administration of SUVN-G3031 produced significant increase in acetylcholine, histamine, dopamine and norepinephrine levels in the cortex. SUVN-G3031 produced wake promoting activity in male Wistar rats. In the present study, effects of SUVN-G3031 on sleep/ wake profile were evaluated in rats with lateral hypothalamic lesion using neurotoxin hypocretin-2-saporin. Narcoleptic-like sleep behavior was observed in rats injected with hypocretin-2-saporin in lateral hypothalamus. SUVN-G3031 produced significant increase in wakefulness with concomitant decrease in rapid eye movement (REM) sleep in these animals. These results are in agreement with electroencephalography (EEG) studies carried out in healthy male Wistar rats. Results from the current study and the neurotransmitter modulations produced by SUVN-G3031 provide a strong basis for the potential of SUVN-G3031 in treatment of sleep related disorders. First in human, Phase 1 studies for SUVN-G3031 are completed underUS IND and SUVN-G3031 has shown desirable pharmacokinetic profile with safety and tolerability in healthy human volunteers. Phase 2 study for narcolepsy is currently being planned.

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

Chew C, Sengelaub DR (2018) Exercise is neuroprotective following partial motoneuron depletion: Run for your dendrites. Neuroscience 2018 Abstracts 761.02 / MM11. Society for Neuroscience, San Diego, CA.

Summary: We have previously demonstrated that partial depletion of motoneurons innervating the quadriceps muscles induces dendritic atrophy in remaining motoneurons. Furthermore, systemic treatment with supplemental androgens is neuroprotective and dendritic atrophy following partial motoneuron depletion is attenuated. Circulating levels of androgens have previously been shown to increase following exercise, and exercise has been demonstrated to be neuroprotective in a variety of other neurodegenerative and injury models. Thus, we hypothesized that allowing animals to exercise following partial motoneuron depletion would produce neuroprotective effects similar to treatment with supplemental androgens. Motoneurons innervating the vastus medialis muscle in adult male rats were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Following saporin injections, some animals were allowed free access to a running wheel attached to their home cages. Four weeks later, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated horseradish peroxidase, and dendritic arbors were reconstructed in three dimensions. Compared with intact normal males, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons. Early data suggests that exercise can completely protect against this dendritic atrophy, with exercised males showing dendritic arbors lengths significantly longer than saporin and testosterone-treated animals, and of similar length to intact normal animals. These findings suggest that exercise may be a viable means of protecting against collateral dendritic atrophy. The upregulation of testosterone release following exercise combined with our previous data showing the neuroprotective effects of androgen treatment suggest that the neuroprotective following exercise may be attributable to systemic androgen upregulation.

Related Products: CTB-SAP (Cat. #IT-14)