References

Tao X, Li N, Liu F, Hu Y, Liu J, Zhang Y-M (2018) In vitro examination of microglia-neuron crosstalk with BV2 cells, and primary cultures of glia and hypothalamic neurons. Heliyon 4:e00730. doi: 10.1016/j.heliyon.2018.e00730 PMID: 30148218

Related Products: Corticotropin Releasing Hormone Rabbit Polyclonal (Cat. #AB-02)

Jo A, Xu J, Deniz S, Cherian S, DeVries SH, Zhu Y (2018) Intersectional strategies for targeting amacrine and ganglion cell types in the mouse retina. Front Neural Circuits 12:66. doi: 10.3389/fncir.2018.00066 PMID: 30186122

Objective: To obtain unambiguous information about retinal processing.

Summary: Results establish a foundation for future application of intersectional strategies in the retina and retino-recipient regions.

Usage: Immunohistochemistry 1:1000.

Related Products: Melanopsin Rabbit Polyclonal (Cat. #AB-N38)

Solari N, Hangya B (2018) Cholinergic modulation of spatial learning, memory and navigation. Eur J Neurosci 48:2199-2230. doi: 10.1111/ejn.14089

Related Products: 192-IgG-SAP (Cat. #IT-01), GAT1-SAP (Cat. #IT-32)

Kosykh A, Beilin A, Sukhinich K, Vorotelyak E (2018) Postnatal neural crest stem cells from hair follicle interact with nerve tissue in vitro and in vivo. Tissue Cell 54:94-104. doi: 10.1016/j.tice.2018.08.005 PMID: 30309515

Objective: To investigate the interaction between Neural crest stem cells that located in the postnatal hair follicle (HF-NCSC) and a nerve tissue (embryonic and adult).

Summary: HF-NCSC maintain their NC potency in the interaction with the embryonic central nerve system tissue. The migration capacity of the HF NCSC corresponds to the developmental stage but not a type of a nerve tissue present in the co-culture. In contrast, an adult brain interaction changes the HF-NCSC status and reduces the proliferation.

Usage: immunohistochemistry (1:50)

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

Pitchers KK, Sarter M, Robinson TE (2018) The hot ‘n’ cold of cue-induced drug relapse. Learn Mem 25:474-480. doi: 10.1101/lm.046995.117

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

Lelkes Z, Abdurakhmanova S, Porkka-Heiskanen T (2018) Cholinergic basal forebrain structures are not essential for mediation of the arousing action of glutamate. J Sleep Res 27:e12605. doi: 10.1111/jsr.12605

Objective: Discover to what extent the cholinergic versus non‐cholinergic basal forebrain projection neurones contribute to the arousing action of glutamate.

Summary: Destruction of the basal forebrain cholinergic neurons did not abolish the wake‐enhancing action of NMDA. Thus, the cholinergic basal forebrain structures are not essential for the mediation of the arousing action of glutamate.

Usage: 0.23 μg 192 IgG‐SAP was administered into the basal forebrain.

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

Oliveira LM, Falquetto B, Moreira TS, Takakura AC (2018) Orexinergic neurons are involved in the chemosensory control of breathing during the dark phase in a Parkinson’s disease model. Exp Neurol 309:107-118. doi: 10.1016/j.expneurol.2018.08.004

Objective: To determine the involvement of orexin cells from the lateral hypothalamus/perifornical area (LH/PeF) on breathing.

Summary: The degeneration of orexinergic neurons in this model of PD can be related to impaired chemoreceptor function in the dark phase.

Usage: For lesions of LH/PeF, two injections of Orexin-B-SAP or Rabbit IgG-SAP (100 ng/μl) were made into the lateral hypothalamus / perifornical area (LH/PeF).

Related Products: Orexin-B-SAP (Cat. #IT-20), Rabbit IgG-SAP (Cat. #IT-35)

Higashi Y, Shimizu T, Yamamoto M, Tanaka K, Yawata T, Shimizu S, Zou S, Ueba T, Yuri K, Saito M (2018) Stimulation of brain nicotinic acetylcholine receptors activates adrenomedullary outflow via brain inducible NO synthase-mediated S-nitrosylation. Br J Pharmacol 175(19):3758-3772. doi: 10.1111/bph.14445 PMID: 30007012

Objective: To examine central mechanisms for the (±)-epibatidine-induced responses, focusing on brain NOS and NO-mediated mechanisms, soluble GC (sGC) and protein S-nitrosylation (a posttranslational modification of protein cysteine thiol groups), in urethane-anaesthetized (1.0 g·kg1, i.p.) male Wistar rats.

Summary: Stimulation of brain nAChRs can induce elevation of plasma catecholamines through brain iNOS-derived NO-mediated protein Snitrosylation in rats. Therefore, brain nAChRs (at least α4β2 subtype) and NO might be useful targets for alleviation of catecholamines overflow induced by smoking.

Usage: Immunohistochemistry (1:1000)

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

Mousseau M, Burma NE, Lee KY, Leduc-Pessah H, Kwok CHT, Reid AR, O’Brien M, Sagalajev B, Stratton JA, Patrick N, Stemkowski PL, Biernaskie J, Zamponi GW, Salo P, McDougall JJ, Prescott SA, Matyas JR, Trang T (2018) Microglial pannexin-1 channel activation is a spinal determinant of joint pain. Sci Adv 4:1-12. doi: 10.1126/sciadv.aas9846

Objective: To identify therapeutic targets for alleviating mechnical allodynia, a sign/symptom of arthritis.

Summary: The pannexin-1 (Panx1) channel is validated as a target; blockade of P2X7 receptors or ablation of spinal microglia prevented and reversed mechanical allodynia.

Usage: Mac-1-SAP and unconjugated Saporin (15 mg per intrathecal injection on days 0, 1, and 2). The specific depletion of spinal lumbar microglia attenuated the development of MIA-induced hypersensitivity indicating that spinal microglia causally contribute to the development of mechanical allodynia. By contrast, intrathecal injection of Control (unconjugated Saporin) did not alter the development of MIA-induced mechanical allodynia.

Related Products: Mac-1-SAP rat (Cat. #IT-33), Saporin (Cat. #PR-01)

Xiong L, Liu Y, Zhou M, Wang G, Quan D, Shuai W, Shen C, Kong B, Huang C, Huang H (2018) Targeted ablation of cardiac sympathetic neurons attenuates adverse post-infarction remodeling and left ventricle dysfunction. Exp Physiol 103:1221-1229. doi: 10.1113/EP086928

Objective: To determine whether targeted ablation of cardiac sympathetic neurons (TACSN) could suppress myocardial infarction-induced adverse cardiac remodeling and left ventricle dysfunction.

Summary: TACSN significantly alleviated sympathetic remodeling and neuroendocrine activation, attenuated cardiac hypertrophy and fibrosis, and improved the left ventricular function. Thus, TACSN may have a beneficial effect on adverse post-infarction remodeling and left ventricle dysfunction.

Usage: 20 μl of CTB-SAP (1.2 mg/ml) was mixed with 4 μl of 3% Evans blue dye to make it visible (CTB-SAP is colorless), ensuring localization within the ganglia. The CTB-SAP/Evans blue dye solution was slowly and intermittently injected into the left stellate ganglia using a glass micropipette.

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