References

Douglas AD, Williams AR, Knuepfer E, Illingworth JJ, Furze JM, Crosnier C, Choudhary P, Bustamante LY, Zakutansky SE, Awuah DK, Alanine DG, Theron M, Worth A, Shimkets R, Rayner JC, Holder AA, Wright GJ, Draper SJ (2014) Neutralization of Plasmodium falciparum merozoites by antibodies against PfRH5. J Immunol 192(1):245-258. doi: 10.4049/jimmunol.1302045 PMID: 24293631

Summary: Plasmodium falciparum is a protozoan parasite that can cause malaria in humans. The human malaria parasite reticulocyte –binding protein homolog 5 (PfRH5) is a potential target for neutralizing antibodies. PfRH5 binds basigin on erythrocytes, and through the use of anti-basigin (Cat. #AB-42), among other antibodies, the authors better characterized aspects of this binding that may be useful in preventing malaria.

Related Products: Antibody to Basigin (Cat. #AB-42)

Takakura AC, Barna BF, Cruz JC, Colombari E, Moreira TS (2014) Phox2b-expressing retrotrapezoid neurons and the integration of central and peripheral chemosensory control of breathing in conscious rats. Exp Physiol 99(3):571-585. doi: 10.1113/expphysiol.2013.076752

Summary: Previous work has shown that lesions to the retrotrapezoid nucleus (RTN) have at least a modest effect on breathing, but it is unclear whether those lesions affected the entire nucleus or were incomplete. The authors used bilateral lesions of the RTN with 0.3 to 1.2 ng total of SSP-SAP (Cat. #IT-11) to eliminate neurokinin-1 receptor-expressing neurons; these are also Phox2b+TH- neurons. The results indicate that loss of Phox2b(+)TH(-) neurons may cause deficits seen after RTN lesion, and help define the ways in which these cells are involved in controlling central and peripheral chemoreflexes.

Related Products: SSP-SAP (Cat. #IT-11)

Freiria-Oliveira AH, Blanch GT, De Paula PM, Menani JV, Colombari DS (2013) Lesion of the commissural nucleus of the solitary tract/A2 noradrenergic neurons facilitates the activation of angiotensinergic mechanisms in response to hemorrhage. Neuroscience 254:196-204. doi: 10.1016/j.neuroscience.2013.09.017

Summary: Previous work has generated conflicting data on the role of catecholaminergic A2 neurons in the nucleus of the solitary tract (NTS) in control of arterial pressure lability. The authors used Anti-DBH-SAP (Cat. #IT-03) to lesion these neurons in a hypotensive hemorrhage model. Rats received two injections of 12.6 ng into the commissural NTS. Mouse IgG-SAP (Cat. #IT-18) was used as a control. The lesioned animals quickly recovered from hypotension, but were impaired by the icv administration of losartan.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

Kinikoglu B, Kong Y, Liao EC (2014) Characterization of cultured multipotent zebrafish neural crest cells. Exp Biol Med (Maywood) 239(2):159-168. doi: 10.1177/1535370213513997 PMID: 24326414

Summary: This work details the isolation of neural crest cells (NCCs) from transgenic zebrafish embryos expressing GFP and flow cytometry; the authors analyzed lineage markers and differentiation of the NCCs. Anti-mu p75 (Cat. #AB-N01AP) was used in immunocytochemistry at a 1:20 dilution on fixed cells.

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

Burke RM, Norman TA, Haydar TF, Slack BE, Leeman SE, Blusztajn JK, Mellott TJ (2013) BMP9 ameliorates amyloidosis and the cholinergic defect in a mouse model of Alzheimer’s disease. Proc Natl Acad Sci U S A 110(48):19567-19572. doi: 10.1073/pnas.1319297110 PMID: 24218590

Summary: During development bone morphogenetic protein 9 (BMP9) induces the cholinergic phenotype in the basal forebrain. The authors investigated the use of BMP9 as a treatment of basal forebrain cholinergic degeneration, such as is seen in Alzheimer’s disease (AD). Transgenic mice displaying AD phenotypes and expressing GFP in cholinergic neurons received icv infusions of BMP9, and several cholinergic markers were assessed. Anti-p75NTR (Cat. #AB-N01) was used in immunoblotting at a 1:3000 dilution to measure p75 levels. The results demonstrate the protective and therapeutic activity of BMP9 on AD symptoms.

Related Products: NGFr (mu p75) Rabbit Polyclonal (Cat. #AB-N01)

Guyenet PG, Stornetta RL, Bochorishvili G, Depuy SD, Burke PG, Abbott SB (2013) C1 neurons: the body’s EMTs. Am J Physiol Regul Integr Comp Physiol 305(3):R187-204 . doi: 10.1152/ajpregu.00054.2013

Summary: Although mainly known for their involvement in the control of arterial pressure, C1 neurons are also suspected to participate in numerous other physiological processes such as neuroendocrine response, glucose homeostasis, food consumption, and others. This review discusses the role of these neurons as ’emergency medical technicians’ – cells that produce and modulate physiological survival responses to acute physical stress. The use of Anti-DBH-SAP (Cat. #IT-03) to delineate C1 neurons in the rostral ventrolateral aspect of the medulla oblongata is discussed.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Leoni G, Rattray M, Fulton D, Rivera A, Butt AM (2014) Immunoablation of cells expressing the NG2 chondroitin sulphate proteoglycan. J Anat 224(2):216-227. doi: 10.1111/joa.12141

Summary: In this work the authors use an antibody against the NG2-glia marker chondroitin sulphate proteoglycan (CSPG) along with Mab-ZAP (Cat. #IT-04) on cell lines and brain slices to eliminate cells expressing CSPG. The results demonstrate selective and effective killing, providing a method to study the function of these cells.

Related Products: Mab-ZAP (Cat. #IT-04)

Romano A, Potes CS, Tempesta B, Cassano T, Cuomo V, Lutz T, Gaetani S (2013) Hindbrain noradrenergic input to the hypothalamic PVN mediates the activation of oxytocinergic neurons induced by the satiety factor oleoylethanolamide. Am J Physiol Endocrinol Metab 305(10):E1266-73. doi: 10.1152/ajpendo.00411.2013

Summary: Feeding behavior and energy balance are in part controlled by signals from the gut. Oleoylethanolamide (OEA) is an acylethanolamide that is thought to play a role in this network. Since peripheral administration of OEA has effects on the nucleus of the solitary tract (NTS) and paraventricular nucleus (PVN) the authors investigated the role of noradrenergic afferent input to these areas. Rats received bilateral 84-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the PVN. Mouse IgG-SAP (Cat. #IT-18) was used as a control.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

Grupe M, Paolone G, Jensen AA, Sandager-Nielsen K, Sarter M, Grunnet M (2013) Selective potentiation of (alpha4)3(beta2)2 nicotinic acetylcholine receptors augments amplitudes of prefrontal acetylcholine- and nicotine-evoked glutamatergic transients in rats. Biochem Pharmacol 86(10):1487-1496. doi: 10.1016/j.bcp.2013.09.005

Summary: Nicotinic acetylcholine receptors (nAChR) are involved in a wide range of processes in the central nervous system, many having to do with higher cognitive functions. In order to better understand how these receptors mediate attentional performance, the authors investigated glutamate release under varying conditions. In one series of experiments rats received a 160-ng injection of 192-IgG-SAP (Cat. #IT-01) into the right medial prefrontal cortex. The resulting decrease in glutamate release after the cholinergic lesion adds to the data indicating that positive modulation of nAChR may help alleviate attentional impairments caused by some brain disorders.

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

Zajo KN, Fadel JR, Burk JA (2013) Assessment of the contributions of baseline performance and prefrontal cortical cholinergic projections to orexin A-induced attentional enhancement. Neuroscience 2013 Abstracts 854.02. Society for Neuroscience, San Diego, CA.

Summary: Orexinergic neurons innervate several brain regions including the basal forebrain, a structure known to be crucial for normal attentional performance in rats. Our previous research demonstrated that orexin receptor blockade impairs attention and that infusions of orexin A into the lateral ventricle enhance attentional performance in animals that have just reached criteria for stable performance levels on a sustained attention task. Our current research investigated whether more highly trained animals show orexin A-induced enhancement of attentional performance and whether basal forebrain cholinergic inputs to the medial prefrontal cortex were necessary for orexin A-induced attentional enhancement. Male FBNF1 hybrid rats were trained in a sustained attention task that required discrimination of visual signals (500, 100 or 25-ms illumination of a central panel light) from trials when no signal was presented. After stable performance levels were established, rats received both intraventricular guide cannula implantation and infusions of either the immunotoxin 192IgG-saporin or vehicle into the medial prefrontal cortex. Postsurgically, rats were retrained to stable performance levels and then received infusions of 0 (vehicle), 10, 100 or 1000pM orexin A in a counterbalanced order prior to task performance. On infusion days, rats were exposed to a version of the task which increased attentional demands by presenting a visual distracter during the middle block of trials within a testing session. In rats trained to higher performance levels, intraventricular orexin A infusions did not significantly enhance attentional performance. Loss of cholinergic projections to the medial prefrontal cortex decreased attentional performance, particularly when a visual distracter was presented. Attentional performance was unaffected in lesioned rats when orexin A was infused into the lateral ventricle. Our findings suggest that orexin A-induced attentional enhancement may be dependent upon baseline performance levels and possibly the integrity of the basal forebrain cholinergic projections to the medial prefrontal cortex.

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