References

Chew C, Sengelaub DR (2021) Exercise is neuroprotective on the morphology of somatic motoneurons following the death of neighboring motoneurons via androgen action at the target muscle. Dev Neurobiol 81(1):22-35. doi: 10.1002/dneu.22794

Objective: To determine where the necessary site of androgen action is for exercise-driven neuroprotective effects on induced dendritic atrophy.

Summary: Exercise following neural injury exerts a protective effect on motoneuron dendrites, which acts via androgen receptor action at the target muscle.

Usage: Motoneurons innervating the left vastus medialis (VM) muscle were selectively killed by intramuscular injection of cholera toxin-conjugated saporin (CTB-SAP).

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

Dezawa S, Nagasaka K, Watanabe Y, Takashima I (2021) Lesions of the nucleus basalis magnocellularis (Meynert) induce enhanced somatosensory responses and tactile hypersensitivity in rats. Exp Neurol 335:113493. doi: 10.1016/j.expneurol.2020.113493

Summary: The authors used 192-IgG-SAP to produce a selective cholinergic lesion in the nucleus basalis of Meynert (NBM) of rats and investigated whether the NBM lesion led to tactile hypersensitivity in the forepaw. Results suggest that neuronal loss in the NBM diminishes acetylcholine actions in the S1, thereby enhancing the cortical representation of sensory stimuli, which may in turn lead to behavioral hypersensitivity.

Usage: The lesion group received injection of 0.3 μL of 192-IgG-SAP into the left nucleus basalis of Meynert (NBM).

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

Puente BR (2021) Chronic pain in dogs (Dolor crónico en el perro). Zaragoza Spain: Gruppo Asis Biomedia, S. L..

Summary: The author presents a thorough overview of aspects of canine chronic pain. He includes SP-SAP (Substance P-Saporin) as an experimental drug, “its use as an adjuvant analgesic in dogs with bone cancer has been studied,”

Related Products: SP-SAP (Cat. #IT-07)

See Also:

• Brown DC et al. Intrathecal substance p-saporin in the dog: efficacy in bone cancer pain. Anesthesiology 119(5):1178-1185, 2013.

Lim I, Mitsui R, Kameda M, Sellers DJ, Chess‐Williams R, Hashitani H (2021) Comparative effects of angiotensin II on the contractility of muscularis mucosae and detrusor in the pig urinary bladder. Neurourol Urodyn 40:102-111. doi: 10.1002/nau.24548 PMID: 33074588

Objective: To explore contractile actions of angiotensin II (AT2) on the muscularis mucosae (MM) of the bladder.

Summary: The MM appears to have great sensitivity to AT2, suggesting that MM may be the predominant target of contractile actions induced by AT2 in the bladder.

Usage: Induction of contractions with Anti-AT2R (1 nM – 1 µM). Immunofluorescence (10-100 pM).

Related Products: Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)

Nelson TS, Taylor BK (2021) Targeting spinal neuropeptide Y1 receptor-expressing interneurons to alleviate chronic pain and itch. Prog Neurobiol 196:101894. doi: 10.1016/j.pneurobio.2020.101894

Summary: Intrathecal administration of NPY-SAP reduced several operant and cognitive measures of Complete Freund’s adjuvant (CFA)-induced allodynia, including responsiveness to cold temperatures, feeding interference, and an escape task, but did not interfere with systemic morphine-induced analgesia. (Wiley et al.) Similar to the spared nerve injury (SNI) model of neuropathic pain, NPY-SAP dose-dependently reduced the development of mechanical allodynia (hindpaw withdrawal response to von Frey filaments), mechanical hyperalgesia (response to blunt pin), and cold allodynia (hindpaw withdrawal response duration to acetone droplet evaporation). (Nelson et al.) Together, these directed lesion studies support the idea that the Y1-IN subpopulation of dorsal horn neurons is necessary for the maintenance of both mechanical and cold modalities of nociceptive transmission in chronic pain states.

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

See Also:

• Wiley RG et al. Neuropeptide Y receptor-expressing dorsal horn neurons: role in nocifensive reflex responses to heat and formalin. Neuroscience 161:139-147, 2009.
• Nelson TS et al. Facilitation of neuropathic pain by the NPY Y1 receptor-expressing subpopulation of excitatory interneurons in the dorsal horn. Sci Rep 9(1):7248, 2019.

Ma X, Fu S, Yin Y, Wu Y, Wang T, Xu G, Liu M, Xu Y, Tian J, Jiang G (2021) Aberrant functional connectivity of basal forebrain subregions with cholinergic system in short-term and chronic insomnia disorder. J Affect Disord 278:481-487. doi: 10.1016/j.jad.2020.09.103

Summary: Previous animal studies have identified the cholinergic basal forebrain (CBF) as a crucial structure in sleep-wake cycle modulation and lesion or inactivation of the BF has been found to increase delta electroencephalogram activity, disturb behavioral arousal, and reduce sleep. They reference Kaur et al. using 192-IgG-SAP to lesion the CBF to examine the role of these neurons in sleep behavior.

See: Kaur S et al. Effects of ibotenate and 192IgG-saporin lesions of the nucleus basalis magnocellularis/substantia innominata on spontaneous sleep and wake states and on recovery sleep after sleep deprivation in rats. J Neurosci 28:491-504, 2008.

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

Zhang C, Shen L, Zhu Y, Xu R, Deng Z, Liu X, Ding Y, Wang C, Shi Y, Bei L, Wei D, Thorne RF, Zhang XD, Yu L, Chen S (2021) KDM6A promotes imatinib resistance through YY1-mediated transcriptional upregulation of TRKA independently of its demethylase activity in chronic myelogenous leukemia. Theranostics 11(6):2691-2705. doi: 10.7150/thno.50571 PMID: 33456567

Objective: To identify histone lysine demethylases (KDMs) with altered expression in chronic myelogenous leukemia (CML) and define their contribution to imatinib resistance.

Summary: KDM6A promotes imatinib-resistance in CML cells. The identification of the KDM6A/YY1/TRKA axis as a novel imatinib-resistance mechanism represents an unexplored avenue to overcome tyrosine kinase inhibitor resistance in CML.

Usage: Western blot

Related Products: trkA Rabbit Polyclonal (Cat. #AB-N03)

Lee TH, Yau SY (2021) From obesity to hippocampal neurodegeneration: Pathogenesis and non-pharmacological interventions. Int J Mol Sci 22(1):201. doi: 10.3390/ijms22010201

Summary: This review provides insights into how chronic metabolic disorders, like obesity, could impair brain health and cognitive functions in later life. The authors reference the use of CCK-SAP into the nodose ganglia to impair spatial memory and contextual episodic memory.

See: Suarez AN et al. Gut vagal sensory signaling regulates hippocampus function through multi-order pathways. Nat Commun 9(1):2181, 2018.

Related Products: CCK-SAP (Cat. #IT-31)

Ringel AE, Drijvers JM, Baker GJ, Catozzi A, García-Cañaveras JC, Gassaway BM, Miller BC, Juneja VR, Nguyen TH, Joshi S, Yao CH, Yoon H, Sage PT, LaFleur MW, Trombley JD, Jacobson CA, Maliga Z, Gygi SP, Sorger PK, Rabinowitz JD, Sharpe AH, Haigis MC (2020) Obesity shapes metabolism in the tumor microenvironment to suppress anti-tumor immunity. Cell 183(7):1848-1866.e26. doi: 10.1016/j.cell.2020.11.009 PMID: 33301708

Objective: To investigate how obesity shifts the metabolic landscape of the tumor microenvironment (TME) to inhibit T cell function and promote tumor growth.

Summary: High-fat diet – induced obesity impairs CD8+ T cell function in the murine TME, accelerating tumor growth.

Usage: Immunoprecipitation

Related Products: Trans-4-Hydroxy-L-Proline Rabbit Polyclonal, Conjugated (Cat. #AB-T044)

Uda M, Yoshihara T, Ichinoseki-Sekine N, Baba T, Yoshioka T (2020) Potential roles of neuronal nitric oxide synthase and the PTEN-induced kinase 1 (PINK1)/Parkin pathway for mitochondrial protein degradation in disuse-induced soleus muscle atrophy in adult rats. PLoS One 15(12):e0243660. doi: 10.1371/journal.pone.0243660 PMID: 33296434

Objective: To investigate the involvement of neuronal nitric oxide synthase (nNOS) and the PINK1/Parkin pathway in soleus muscle atrophy induced by 14 days of hindlimb unloading (HU) in adult rats.

Summary: Excessive NO is not produced in atrophied soleus muscles despite nNOS accumulation, suggesting that excessive NO dose not mediate in soleus muscle atrophy at least after 14 days of HU.

Usage: Western blot (1:1000)

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