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NGFR


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  • Nerve growth factor regulates dopamine D(2) receptor expression in prolactinoma cell lines via p75(NGFR)-mediated activation of nuclear factor-kappaB. 11818506

    Two groups of prolactinoma cell lines were identified. One group (responder) expresses both D(2) dopamine receptors and an autocrine loop mediated by nerve growth factor (NGF) and one group (nonresponder) lacks both D(2) receptors and NGF production. D(2) receptor expression in these cell lines is dependent on NGF. Indeed, NGF inactivation in responder cells decreases D(2) receptor density, while NGF treatment induces D(2) receptor expression in nonresponders. Here we show that inactivation of p75(NGFR), but not of trkA, resulted in D(2) receptor loss in responder cells and prevented D(2) receptor expression induced by NGF in the nonresponder. Analysis of nuclear factor-kappaB (NF-kappaB) nuclear accumulation and binding to corresponding DNA consensus sequences indicated that in NGF-secreting responder cells, but not in nonresponders, NF-kappaB is constitutively activated. Moreover, NGF treatment of nonresponder cells induced both nuclear translocation and DNA binding activity of NF-kappaB complexes containing p50, p65/RelA, and cRel subunits, an effect prevented by anti-p75(NGFR) antibodies. Disruption of NF-kappaB nuclear translocation by SN50 remarkably impaired D(2) receptor expression in responder cells and prevented D(2) gene expression induced by NGF in nonresponders. These data indicate that in prolactinoma cells the effect of NGF on D(2) receptor expression is mediated by p75(NGFR) in a trkA-independent way and that NGF stimulation of p75(NGFR) activates NF-kappaB, which is required for D(2) gene expression. We thus suggest that NF-kappaB is a key transcriptional regulator of the D(2) gene and that this mechanism may not be confined to pituitary tumors, but could also extend to other dopaminergic systems.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    AB1554
    Produktbezeichnung:
    Anti-Nerve Growth Factor Receptor Antibody, p75

  • Immuno-electron microscopy characterization of human bone marrow stromal cells with anti-NGFR antibodies. 8846047

    Human bone marrow stromal cells have been examined with an immuno-electron microscopy technique in order to better define their structure and function in normal hematopoiesis. Bone marrow fragments from normal donors, after mild permeabilization and glutaraldehyde prefixation were labeled with the Me20.4 Mab, which recognizes the low affinity nerve growth factor (NGFR) and was recently described as specifically identifying fibroblastic-like bone marrow stromal cells. Five nm gold immuno-conjugates served as markers. NGFR+ cells were showing either a star-shape, with long and convoluted dendritic projections, and branching with each other to form a complex system of lacunae upon which hematopoietic cells were arranged. Other NGFR+ cells had an elongated spindle-like morphology. NGFR+ dendrites were seen in close contact with each other and with the different hematopoietic cells, although definite junctions were never noticed. NGFR+ dendrites were also observed surrounding mature plasma cells, in close apposition with adipocytes or surrounding bone marrow sinusoids. These findings may give some clues about the function of the bone marrow stromal cells, which are known to be involved in the homing and recirculation of hemopoietic cells; in addition, the presence and distribution of NGFR in the bone marrow stroma may support the recent evidence of a co-stimulatory effect of NGF in early hematopoiesis.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    05-446
    Produktbezeichnung:
    Anti-p75NTR (Neurotrophin Receptor) Antibody, clone ME20.4

  • Survival of cholinergic forebrain neurons in developing p75NGFR-deficient mice. 8939868

    The functions of the low-affinity p75 nerve growth factor receptor (p75(NGFR)) in the central nervous system were explored in vivo. In normal mice, approximately 25 percent of the cholinergic basal forebrain neurons did not express TrkA and died between postnatal day 6 and 15. This loss did not occur in p75(NGFR)-deficient mice or in normal mice systemically injected with a p75(NGFR)-inhibiting peptide. Control, but not p75(NGFR)-deficient, mice also had fewer cholinergic striatal interneurons. Apparently, p75(NGFR) mediates apoptosis of these developing neurons in the absence of TrkA, and modulation of p75(NGFR) can promote neuronal survival. Cholinergic basal forebrain neurons are involved in learning and memory.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    AB143
    Produktbezeichnung:
    Anti-Choline Acetyltransferase (ChAT) Antibody

  • Differential effects on spatial navigation of immunotoxin-induced cholinergic lesions of the medial septal area and nucleus basalis magnocellularis. 8027790

    The effects on anatomy and behavior of a ribosomal inactivating protein (saporin) coupled to a monoclonal antibody against the low-affinity NGF receptor (NGFr) were examined. In adult rats, NGFr is expressed predominantly in cholinergic neurons of the medial septal area (MSA), diagonal band nuclei, and nucleus basalis magnocellularis (nBM), but also in noncholinergic cerebellar Purkinje cells. Rats with immunotoxin injections to the MSA, nBM, and lateral ventricle were compared to controls on a spatial and cued reference memory task in the Morris maze. Toxin injections to the MSA slightly impaired the initial, but not asymptotic, phase of spatial navigation. Injections to the nBM impaired all phases of spatial navigation. Cued navigation, however, was not affected in either the MSA or nBM group. The ventricular injections severely affected spatial and cued navigation. Acetylcholinesterase (AChE) histochemistry and NGFr and choline acetyltransferase immunohistochemistry revealed a loss of (1) almost all NGFr-positive cholinergic neurons in the MSA and AChE fibers in hippocampus (MSA group); (2) almost all NGFr neurons in the nBM, some in the MSA, most AChE fibers in neocortex and some in the hippocampus (nBM group), and (3) almost all NGFr neurons in the MSA and nBM and their corresponding hippocampal and cortical AChE fibers (ventricular group). Cholinergic nBM projections to the amygdala were largely preserved in all groups. The amount of cholinergic fiber loss in the cortex correlated modestly, but significantly, with the severity of impairment of the asymptotic phase of performance of the spatial task. An unambiguous interpretation of the anatomical locus of behavioral deficits was not possible because of damage to cholinergic striatal interneurons (nBM group) and to noncholinergic cerebellar Purkinje cells (ventricular group). These data suggest that the cholinergic cortical system is critical to the performance of this spatial memory task. Cholinergic denervation of the hippocampus alone, however, is not sufficient to impair markedly performance of this task.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    Mehrere
    Produktbezeichnung:
    Mehrere

  • Complete and selective cholinergic denervation of rat neocortex and hippocampus but not amygdala by an immunotoxin against the p75 NGF receptor. 8120624

    The immunotoxin 192 IgG-saporin, produced by coupling the ribosome-inactivating protein saporin to the monoclonal 192 IgG antibody against the low-affinity p75 NGF receptor (NGFr), was injected into the cerebral ventricle, septal area, and substantia innominata of adult rats. Injections into the cerebral ventricle induced a complete loss of NGFr-positive basal forebrain neurons and their axons. Extensive loss of cholinergic neurons was found in the septum, diagonal band, and magnocellular preoptic nucleus but not in the nucleus basalis-substantia innominata complex, where many cholinergic, presumably NGFr-negative, neurons remained intact. Cholinergic fibers were completely lost in the neocortex and hippocampus, showed some preservation in allocortical areas, and showed only minor loss in the amygdala. The NGFr-positive cholinergic basal forebrain neurons progressively degenerated during the first 5 d and did not recover after 180 d. The effect of intraventricular 192 IgG-saporin injections on NGFr-positive basal forebrain neurons could be blocked by simultaneous intraventricular injection of colchicine. Intraparenchymal injections into the septal area or substantia innominata damaged cholinergic neurons mainly around the injection sites and reduced their respective cortical and hippocampal projections. Noncholinergic septal neurons containing parvalbumin and noncholinergic neurons containing calbindin-D28k or NADPHd, which were adjacent to cholinergic nucleus basalis-substantia innominata neurons, were not affected by 192 IgG-saporin. The ChAT immunoreactivity in cortical interneurons, habenula, and brainstem was unchanged. Dopaminergic and noradrenergic cortical afferents remained intact. 192 IgG-saporin damaged two neuronal groups outside the basal forebrain that express the p75 NGF receptor: NGFr-positive cerebellar Purkinje cells after intraventricular injection and cholinergic striatal interneurons after injections into the substantia innominata. These results indicate that the immunotoxin 192 IgG-saporin induces a complete and selective lesion of NGFr-positive cholinergic basal forebrain neurons projecting to hippocampus and neocortex.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    Mehrere
    Produktbezeichnung:
    Mehrere

  • Nerve growth factor (NGF) reverses axotomy-induced decreases in choline acetyltransferase, NGF receptor and size of medial septum cholinergic neurons. 2558781

    Intraventricular nerve growth factor (NGF) infusion in the adult rat can prevent and also, if delayed, reverse the disappearance of most of the axotomized medial septum cholinergic neurons immunostained for choline acetyltransferase (ChAT). We have utilized the delayed NGF treatment protocol to (i) extend to 3 months the delay time between axotomy and NGF treatment, (ii) define the time course of their recovery, (iii) determine that immunostaining for the (lower affinity) NGF receptor (NGFR) parallels loss and reversal of the ChAT marker, and (iv) evaluate changes in cholinergic somal size following axotomy and subsequent NGF treatment. While NGF treatments starting only 7 days after the fimbria-fornix transection (axotomy) almost entirely restored the number of both ChAT- and NGFR-positive medial septum neurons, longer delayed (2-3 weeks) treatment brought about recovery from the baseline of 20-25% to only about 70% of the control numbers. This limited recoverability, however, persisted even after a 95 day delay period. In all cases examined maximal recoveries were achieved within 3-7 days of NGF treatment. Neuronal size analyses provided evidence for an axotomy-induced atrophy. NGF treatments, started with 1 or 2 week delays, not only reversed fully the average somal size loss but also induced an actual hypertrophy of several of those neurons. These results provide additional evidence that at least half of the apparent loss of cholinergic medial septum neurons upon axotomy is due to a loss of markers such as the transmitter-related enzyme ChAT and NGFR rather than to actual neuronal cell death. These results also show that NGF exerts a genuine trophic influence by regulating the size of its target neurons as well as their content of several proteins.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    MAB305
    Produktbezeichnung:
    Anti-Choline Acetyltransferase Antibody, clone 1E6