References

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)

Kohli S, King MV, Williams S, Edwards A, Ballard TM, Steward LJ, Alberati D, Fone KCF (2019) Oxytocin attenuates phencyclidine hyperactivity and increases social interaction and nucleus accumben dopamine release in rats. Neuropsychopharmacology 44(2):295-305. doi: 10.1038/s41386-018-0171-0

Summary: The authors suggest that further evaluation such as by microinjection with selective antagonists or lesions using the neurotoxin, Oxytocin-SAP, would help delineate the brain region/s and receptor/s involved.

Related Products: Oxytocin-SAP (Cat. #IT-46)

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)

Matamoros AJ (2018) Microtubule-mediated nerve regeneration: Knocking down the microtubule severing protein fidgetin augments nerve regeneration in vitro and in vivo. Drexel University Thesis.

Objective: To explore the effects of fidgetin knockdown in adult dorsal root ganglia both in vitro and in vivo.

Summary: In vitro: fidgetin knockdown in adult dorsal root ganglia neurons increases a specific domain of microtubule mass responsible for expanding microtubules, increases the length of axons on and off the inhibitory spots, and promotes cellular growth on and across the inhibitory spots. In vivo: fidgetin augments nerve regeneration in vivo, thus highlighting fidgetin as a novel therapeutic target to augment nerve regeneration

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

Kucharczyk M, Kurek A, Pomierny B, Detka J, Papp M, Tota K, Budziszewska B (2018) The reduced level of growth factors in an animal model of depression is accompanied by regulated necrosis in the frontal cortex but not in the hippocampus. Psychoneuroendocrinology 94:121-133. doi: 10.1016/j.psyneuen.2018.05.008 PMID: 29775875

Objective: To investigate if the different types of stress alter neuronal plasticity markers distinctively in the frontal cortex (FCx) and in the hippocampus (Hp).

Summary: The authors concluded that chronic stress during pregnancy can result in serious alterations in the functioning of the FCx of the progeny, facilitating the development of depressive behavior later in life. They also suggest that the altered energy metabolism may redirect pro-NGF/p75NTR/ATF2 signaling in the cortical neurons towards cellular death resembling regulated necrosis, rather than apoptosis.

Usage: Western blot (1:1000)

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

Bhat SA, Sood A, Shukla R, Hanif K (2019) AT2R activation prevents microglia pro-inflammatory activation in a nox-dependent manner: Inhibition of PKC activation and p47(PHOX) phosphorylation by PP2A. Mol Neurobiol 56(4):3005-3023. doi: 10.1007/s12035-018-1272-9 PMID: 30076526

Objective: To investigate the involvement of AT2R in NADPH oxidase (NOX)-mediated microglia activation.

Summary: AT2R, via PP2A-mediated inhibition of PKC, prevents the NOX activation, ROS generation, and subsequent pro-inflammatory activation of microglia.

Usage: Immunoblotting: membranes were incubated with respective primary antibodies AT1R (1:1000), AT2R (1:500). Immunocytochemistry: AT1R (1:100), AT2R (1:100).

Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP), Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)