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)

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)

Goodman RL, Lopez JA, Bedenbaugh MN, Connors JM, Hardy SL, Hileman SM, Coolen LM, Lehman MN (2018) Evidence that the LH surge in ewes involves both neurokinin B-dependent and -independent actions of kisspeptin. Neuroscience 2018 Abstracts 773.20 / YY14. Society for Neuroscience, San Diego, CA.

Summary: It is generally recognized that kisspeptin plays a key role in induction of the LH surge in sheep and we have reported evidence that neurokinin B (NKB) does so as well. Specifically, disrupting NKB signaling in the retrochiasmatic area (RCh) using either an antagonist to its receptor, NK3R, or lesions of NK3R-containing neurons in the RCh with a saporin conjugate (NK3-SAP) reduced the amplitude of the estrogen-induced LH surge by 50%. Because a KISS1R antagonist (p271) also produced a 50% decrease in surge amplitude, we hypothesized that these two systems are organized in series with NKB actions in the RCh stimulating kisspeptin release. If this is the case, then the combination of NK3R lesions and a KISS1R antagonist should produce the same inhibition as either treatment alone. This experiment tested this prediction using a 2 x 2 design. Breeding season ewes were ovariectomized and immediately given an estradiol (E) implant sc and two progesterone implants (CIDRs) intravaginally that produced luteal phase levels of these steroids. Ewes then received bilateral injections of either NK3-SAP (n=6) or Blank-SAP (n=5) into the RCh. Three weeks later, an artificial follicular phase was produced by inserting four 3 cm long E implants 24 hrs after CIDR removal and either saline or p271 was infused into the lateral ventricle for 16-24 hrs after E implantation; LH was monitored every 2-4 hrs for two days. CIDRs were then reinserted and the protocol repeated in a cross-over design so that all ewes received saline and p271 treatment. In Blank-SAP ewes, p271 decreased the peak of the LH surge from 61.2 ± 7.6 to 27.4 ± 4.6 ng/mL and delayed it 8 hrs (from 26.5 ± 0.5 to 34.1 ± 1.2 hrs post E implantation). The NK3-SAP injections alone decreased the peak of the LH surge to 29.7 ± 10.7 ng/mL compared to Blank-SAP, but the peak was not further inhibited by p271 in these NK3-SAP-treated ewes (24.4 ± 1.4 ng/mL). However, p271 delayed the peak of the LH surge (from 28.8 ± 1.2 to 34.8 ± 2.1 hrs post E implantation) in the ewes injected with NK3-SAP. Based on these results, we propose that kisspeptin has two roles in the LH surge in ewes: it initiates the surge independent of NKB signaling in the RCh, and maintains LH secretion during the surge by a NKB-dependent system.

Related Products: NKB-SAP (Cat. #IT-63), Blank-SAP (Cat. #IT-21)