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Minocycline protects basal forebrain cholinergic neurons from mu p75-saporin immunotoxic lesioning.
Hunter CL, Quintero EM, Gilstrap L, Bhat NR, Granholm AC (2004) Minocycline protects basal forebrain cholinergic neurons from mu p75-saporin immunotoxic lesioning. Eur J Neurosci 19(12):3305-3316. doi: 10.1111/j.0953-816X.2004.03439.x
Summary: In Alzheimer’s disease basal cholinergic degeneration is accompanied by glial activation and the release of pro-inflammatory cytokines. To investigate whether neural events other than degeneration can cause effects of Alzheimer’s disease, the authors treated mice with minocycline after lesioning the basal forebrain with 3.6 µg of mu p75-SAP (Cat. #IT-16). Administration of minocycline reduced the loss of cholinergic neurons, reduced glial response to the lesion, and lessened the cognitive impairment due to mu p75-SAP lesions.
Related Products: mu p75-SAP (Cat. #IT-16)
NADPH oxidase contributes to angiotensin II signaling in the nucleus tractus solitarius.
Wang G, Anrather J, Huang J, Speth RC, Pickel VM, Iadecola C (2004) NADPH oxidase contributes to angiotensin II signaling in the nucleus tractus solitarius. J Neurosci 24(24):5516-5524. doi: 10.1523/JNEUROSCI.1176-04.2004 PMID: 15201324
Objective: To investigated whether NADPH oxidase is involved in angiotensin II signaling in central autonomic neurons.
Summary: Angiotensin II (AngII), acting through angiotensin type 1 (AT1 ) receptors, exerts powerful effects on central autonomic networks regulating cardiovascular homeostasis and fluid balanceColocalization of AT-1r’s and a NADPH oxidase subunit provides evidence that NADPH oxidase is involved in the effects of angiotensin II on autonomic neurons.
Usage: Immunolabeling (1:200)
Related Products: Angiotensin II receptor (AT-1AR) Rabbit Polyclonal, affinity-purified (Cat. #AB-N25AP), Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP), Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)
Exogenous testosterone prevents motoneuron atrophy induced by contralateral motoneuron depletion.
Fargo KN, Sengelaub DR (2004) Exogenous testosterone prevents motoneuron atrophy induced by contralateral motoneuron depletion. J Neurobiol 60(3):348-359. doi: 10.1002/neu.20027
Summary: Gonadal steroids have been shown to supply a variety of neuroprotective and neurotherapeutic effects. Using 1-µl injections of 0.1% CTB-SAP (Cat. #IT-14) into the ipsalateral bulbocavernosus and the levator ani of rats, the authors examined the protective effects of testosterone on motoneuron morphology. After the lesion was induced some rats were castrated, and all animals were treated with exogenous testosterone. The results suggest that high-normal levels of testosterone can prevent motoneuron atrophy induced by contralateral motoneuron depletion.
Related Products: CTB-SAP (Cat. #IT-14)
Decreased neurogenesis after cholinergic forebrain lesion in the adult rat.
Cooper-Kuhn CM, Winkler J, Kuhn HG (2004) Decreased neurogenesis after cholinergic forebrain lesion in the adult rat. J Neurosci Res 77(2):155-165. doi: 10.1002/jnr.20116
Summary: Adult mammalian brains can produce new neurons, mainly in two areas: the interconnected system of the lateral ventricle and the olfactory bulb, and the dentate gyrus of the hippocampus. The authors used a 3.5 µg-injection of 192-Saporin (Cat. #IT-01) into the right ventricle of rats to determine whether cholinergic input is necessary for adult neurogenesis. The results suggest that acetylcholine, a product of cholinergic neurons, is necessary for the survival of newly-formed neurons.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Selective lesioning of the cholinergic septo-hippocampal pathway does not disrupt spatial short-term memory: a comparison with the effects of fimbria-fornix lesions.
Winters BD, Dunnett SB (2004) Selective lesioning of the cholinergic septo-hippocampal pathway does not disrupt spatial short-term memory: a comparison with the effects of fimbria-fornix lesions. Behav Neurosci 118(3):546-562. doi: 10.1037/0735-7044.118.3.546
Summary: The authors wished to investigate the role of the cholinergic system of the basal forebrain in delayed matching (DMTP)- and nonmatching (DNMTP)-to-position tasks after bilateral injections of 0.035 µg of 192-Saporin (Cat. #IT-01) into the dorsal and ventral hippocampus. The treated animals were compared to rats given fimbria-fornix (FF) lesions. Only the FF-lesioned animals showed impairment on DMTP and DNMTP tasks, demonstrating that the cholinergic septohippocampal system is not required for successful DMTP or DNMTP performance.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Immunotoxins and neuropeptide-toxin conjugates experimental applications.
Lappi DA, Wiley RG (2004) Immunotoxins and neuropeptide-toxin conjugates experimental applications. Mini Rev Med Chem 4(5):585-595. doi: 10.2174/1389557043403882
Summary: The use of targeted toxins in research is rich and varied; here the authors describe some of the exciting results that researchers have made in the neurosciences.
A cell-surface molecule selectively expressed on murine natural interferon-producing cells that blocks secretion of interferon-alpha.
Blasius A, Vermi W, Krug A, Facchetti F, Cella M, Colonna M (2004) A cell-surface molecule selectively expressed on murine natural interferon-producing cells that blocks secretion of interferon-alpha. Blood 103(11):4201-4206. doi: 10.1182/blood-2003-09-3108
Objective: To demonstrate the recruitment and function of natural interferon (IFN)-producing cells (IPCs) in murine infection models.
Summary: Incubation of IPCs with the antibody in vitro or administration of the antibody in vivo dramatically reduce secretion of IFN-α in response to deoxycytidylate-phosphatedeoxyguanylate (CpG) DNA without causing IPC depletion. Thus, the antibody identifies an IPC-specific surface molecule that, when engaged, inhibits IFN-α secretion.
Usage: Biotinylated 440c antibody mixed with Streptavidin-ZAP was applied to bone marrow-derived IPCs. Approximately 70% of CD11c+ B220hi 440c bright IPCs were depleted from culture within 36 hours.
Related Products: Streptavidin-ZAP (Cat. #IT-27)
Corticotropin-releasing hormone (CRH) requirement in Clostridium difficile toxin A-mediated intestinal inflammation.
Anton PM, Gay J, Mykoniatis A, Pan A, O’Brien M, Brown D, Karalis K, Pothoulakis C (2004) Corticotropin-releasing hormone (CRH) requirement in Clostridium difficile toxin A-mediated intestinal inflammation. Proc Natl Acad Sci U S A 101(22):8503-8508. doi: 10.1073/pnas.0402693101 PMID: 15159534
Related Products: Corticotropin Releasing Hormone Rabbit Polyclonal (Cat. #AB-02)
Effects of hypocretin2-saporin and antidopamine-beta-hydroxylase-saporin neurotoxic lesions of the dorsolateral pons on sleep and muscle tone.
Blanco-Centurion C, Gerashchenko D, Salin-Pascual RJ, Shiromani PJ (2004) Effects of hypocretin2-saporin and antidopamine-beta-hydroxylase-saporin neurotoxic lesions of the dorsolateral pons on sleep and muscle tone. Eur J Neurosci 19(10):2741-2752. doi: 10.1111/j.0953-816X.2004.03366.x
Summary: Narcolepsy is linked to the loss of orexin (or hypocretin)-containing neurons in the brain. These neurons are located in the perifornical region of the posterior hypothalamus and innervate the locus coeruleus (LC). To investigate the role of the LC in sleep the authors injected 0.3 µl of 192-Saporin (Cat. IT-01) or anti-DBH-SAP (Cat. #IT-03) at 1 µg/µl. They also used 0.3 µl of orexin-SAP (Cat. #IT-20) at either 90 ng/µl or 60 ng/µl in a separate group of animals. The results indicate that orexin innervation to the pons plays a role in arousal from sleep.
Related Products: 192-IgG-SAP (Cat. #IT-01), Anti-DBH-SAP (Cat. #IT-03), Orexin-B-SAP (Cat. #IT-20)
Glucoprivation increases expression of neuropeptide Y mRNA in hindbrain neurons that innervate the hypothalamus.
Li AJ, Ritter S (2004) Glucoprivation increases expression of neuropeptide Y mRNA in hindbrain neurons that innervate the hypothalamus. Eur J Neurosci 19(8):2147-2154. doi: 10.1111/j.1460-9568.2004.03287.x
Summary: It is suspected that hypothalamic neuropeptide Y (NPY) innvervation of the hypothalamus contributes to glucoregulatory feeding. Along with mRNA studies, the authors injected 42 ng of anti-DBH-SAP (Cat. #IT-03) into the paraventricular nucleus. Elimination of the hindbrain catecholamine/NPY neurons abolished increases in NPY expression due to glucoprivic conditions. This response suggests that NPY hindbrain neurons play a role in glucoprivic feeding and other glucoregulatory responses.
Related Products: Anti-DBH-SAP (Cat. #IT-03)
