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Biomedical subjects

L Aloe

Publications and source records attributed to L Aloe.

At least 217 records · Page 12Linked to original sources
PubMed1975

Nerve growth factor induces volume increase and enhances tyrosine hydroxylase synthesis in chemically axotomized sympathetic ganglia of newborn rats.

Concomitant daily treatment of newborn rats for a 2-week to 1-month period with 10 mug/g of body weight of nerve growth factor and 100 mug/g of body weight of 6-hydroxydopamine produces in the cell bodies of adrenergic neurons the characteristic effects of the growth factor but in the nerve terminals the characteristic effects of 6-hydroxydopamine. The dual opposite effects result in a striking volume increase of sympathetic ganglia which far exceeds that produced by nerve growth factor alone. The selective induction of tyrosine hydroxylase [L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] in these chemically axotomized adrenergic neurons is even more pronounced than that produced by nerve growth factor alone in intact neurons.

Animals↗
PubMed1975

Light and electron microscopic studies on the excessive growth of sympathetic ganglia in rats injected daily from birth with 6-OHDA and NGF.

Concomitatn daily treatment of rats immediately after birth with NGF and 6-OHDA for a period of 2-4 weeks, results in a volume increase of sympathetic ganglia of thirty times that of controls and 2.3 that of NGF treated littermates, at three weeks of age. Studies at the light, fluorescent and electron-microscope, showed that this overall enlargement is due to increase in size and number of sympathetic neurons and, to an even higher extent, to profuse production and branching of collaterals from postganglionic adrenergic nerve fibers. These axonal collaterals find accomodation inside the ganglia where they displace nerve cells and build a thick fibrillar capsule around the same ganglia. The survival in excellent conditions of sympathetic nerve cells treated with NGF but prevented by 6-OHDA from establishing anatomical and functional connections with their end organs, suggests that the growth factor find access to its target cells through the plasms membrane which envelops the cell perikarya. The extraordinary production of collaterals by chemically axotomized sympathetic fibers, brings to light growth potentialities of these fibers which materialize only upon disconnection of their endings from peripheral tissues. These results uncover a new facet of the interaction between nerve fibers and innervated tissues.

Animals↗
PubMed1973

Mechanism of action of nerve growth factor and cyclic AMP on neurite outgrowth in embryonic chick sensory ganglia: demonstration of independent pathways of stimulation.

The suggested role of adenosine 3':5'-cyclic monophosphate as the "second messenger" in the neurite outgrowth from chick embryonic sensory ganglia mediated by nerve growth factor was examined. Although N(6),O(2)-dibutyryl adenosine 3':5'-cyclic monophosphate induces fiber outgrowth at concentrations of 1-5 mM, this response is morphologically distinct from that produced by nerve growth factor, is pH dependent, is mimicked by sodium butyrate, and does not occur in sympathetic ganglia. In addition, nerve growth factor does not alter the amounts of intracellular cyclic AMP during incubations up to 24 hr and does not stimulate adenylate cyclase in broken-cell preparations. Addition of theophylline, an inhibitor of phosphodiesterase, causes increases in intracellular levels of cyclic AMP but does not affect fiber outgrowth. These observations indicate that the nerve growth factor response is not mediated through cyclic AMp and that stimulation of sensory ganglia by exogenous cyclic AMP derivatives is probably of limited physiological significance. These findings are also compatible with the developing hypothesis, based on structural similarities, that nerve growth factor and insulin exert their effects on their respective responsive tissues by related mechanisms.

Adenylyl Cyclases↗
PubMedDate not supplied

Nerve growth factor: a neurotrophin with activity on cells of the immune system.

Numerous studies published in the last two decades provide evidence that nerve growth factor (NGF), a polypeptide originally discovered because of its neurotrophic activity, acts on a variety of cells of the immune system, including mast cells, eosinophils, and B and T lymphocytes. NGF has been shown to increase during inflammatory responses, autoimmune disorders, parasitic infections, and allergic diseases. Moreover, stress, which is characterized also by activation of a variety of immune cells, causes a significant increase in basal plasma NGF levels. Recently published studies reveal that hematopoietic progenitor cells seem to be able to produce and/or respond to NGF. We report these data and discuss the hypothesis of the possible implication of NGF on the functional activities of immune cells.

Animals↗
PubMedDate not supplied

Nerve growth factor plasma levels and ventricular repolarization in Rett syndrome.

Rett syndrome is a severe neurological developmental disorder. In this syndrome, the high incidence of sudden death is correlated with an alteration of ventricular repolarization. The purpose of this study was to evaluate plasmatic levels of nerve growth factor (NGF) in Rett patients with prolonged corrected QT (QTc) interval in comparison with those of Rett patients with normal QTc. We observed 23 female Rett patients (9.9+/-4.7 years). NGF plasma levels and QTc interval were measured in all patients. Student t-test was performed for statistical analysis. NGF plasma levels were significantly lower in Rett patients with QTc interval prolongation (QTc > 0.44 sec) in comparison with Rett patients with a normal QTc interval (4.5+/-4.5 vs 11+/-8.3 pg/ml, p = 0.02). The alteration of NGF levels, observed in Rett patients with a long QTc interval, may explain the presence of an altered ventricular repolarization associated with a higher risk of cardiac arrhythmias.

Adolescent↗
PubMedDate not supplied

Human lung fibroblast response to NGF, IL-1beta, and dexamethsone.

It has been shown that lung mast cells, eosinophils, and fibroblasts are receptive to the action of nerve growth factor (NGF) and that NGF is released in to the bloodstream of subjects affected by allergic inflammatory response. The role of NGF in lung inflammatory disorders is unclear because there is evidence suggesting that NGF can be involved in both proinflammatory and anti-inflammatory responses. Lung fibroblasts play a marked role in inflammation. In this study we investigated the effect of NGF, interleukin 1beta (II-1beta), and dexamethasone (DEX) on human lung fibroblasts in vitro. We found that II-1beta, but not NGF, promotes fibroblasts' survival and that NGF stimulates trkA receptor expression, down regulates TFG-alpha, and has no effect on TNF-beta immunoreactivity. Moreover, DEX exerts different effects on NGF release by fibroblasts pre-exposed to II-1gamma. Our findings suggest that the NGF released by lung fibroblast during inflammation is not associated with the increase of proinflammatory factors such as TNF-alpha and II-1beta.

Animals↗
PubMedDate not supplied

Levels of NGF, p75NGFR and ChAT immunoreactivity in brain of adult and aged microencephalic rats.

Methylazoxymethanol (MAM)-induced microencephalic aged animals with reduced cortical mass and unmodified basal nucleus were used to study the relationship between cells that produce and cells that utilize NGF. Total cortical ChAT activity of MAM 2, 19 and 27 month old animals was reduced compared to their age-matched controls. To verify whether the reduction of enzyme activity can be ascribed to changes in or ablation of projecting neurons, we carried out immunohistochemical analysis of ChAT and low affinity NGF receptor (p75NGFR) in the basal nucleus of control and MAM-treated animals. ChAT and p75NGFR immunostaining of basal forebrain cholinergic neurons showed morphological changes in MAM animals, as revealed by cellular atrophy, reduced dendritic arborization and decreased staining intensity. In the cerebral cortex of microencephalic animals, reduced levels of NGF compared to controls were observed at all examined ages. These results suggest that MAM treatment induces long-lasting ablation of cortical NGF-synthesizing cells leading to reduced trophic support to basal forebrain cholinergic neurons, which might be responsible for the cellular atrophy observed in the basal nucleus.

Aging↗
PubMedDate not supplied

The effect of long-term alcohol intake on brain NGF-target cells of aged rats.

It was reported that chronic exposure to ethanol causes a loss of hippocampal pyramidal cells and of brain cholinergic neurons in both laboratory animals and humans. In the present study, it was hypothesized that nerve growth factor (NGF), a trophic agent for the survival and maintenance of basal forebrain cholinergic neurons (FCN), might be affected by the neurodegenerative events which occur during ethanol consumption. To test this hypothesis, we used aged rats (14 months) exposed for 16 weeks to 40 g/kg per day of undiluted wine. Our experiments showed that chronic alcohol consumption causes a reduction of NGF in the hippocampus (HI) and of choline acetyltransferase (ChAT) activity in both the septum and the HI and a reduction in the distribution of NGF-receptors (NGF-R) in the septum and nucleus of Meynert. Intracerebral injection of NGF in alcohol-exposed rats results in a return to normal levels of ChAT enzymatic activity and NGF-R expression. These experiments indicate that the damaging effect of alcohol on the FCN is also associated with impairment of central NGF-target structures.

Aging↗
PubMedDate not supplied

Nerve growth factor influences neurobehavioral development of newborn mice.

Thirty-six male pups of the CD-1 outbred strain received from postnatal day 2 to day 10 a daily subcutaneous injection of either highly purified murine Nerve Growth Factor (NGF; 5 mg/kg), cytochrome c (5 mg/kg), or saline solution. NGF-treated pups showed a slight, but significant, reduction in body weight gain and a concomitant acceleration in the appearance of early signs of neurobehavioral maturation such as righting reflex, cliff aversion, and response to tactile stimulation of the perioral area. Other responses, including the ultrasonic vocalization pattern on day 7, were unaffected or affected to a lesser extent.

Animals↗
PubMedDate not supplied

Prenatal exposure to methylazoxymethanol acetate in the rat alters neurotrophin levels and behavior: considerations for neurodevelopmental diseases.

We did a single injection of methylazoxymethanol acetate (MAM) in pregnant rats on gestational day (GD) 11 or 12 to investigate the long-lasting effects of early entorhinal cortex (EC) and hippocampus maldevelopment on behavior, brain nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) levels, and the neurotrophin receptor p75 and choline acetyltransferase (ChAT) immunoreactivity. Adult animals treated with MAM had compromised EC development and showed changes in locomotion and displacement activities. In addition, rats treated on GD 12 had increased concentration of NGF and BDNF in the EC and hippocampus if compared to control rats. Prenatal MAM administration did not affect significantly p75 and ChAT distribution in the EC and septum. Results are discussed in reference to the neurodevelopmental hypothesis of psychiatric disorders.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

Prenatal ethanol effects on NGF level, NPY and ChAT immunoreactivity in mouse entorhinal cortex: a preliminary study.

It has been reported that maternal ethanol consumption leads to deficits in the limbic areas involved in cognitive functions and interferes with synthesis and utilization of neurotrophins. In the present study, it was hypothesized that prenatal alcohol intake might induce neuroanatomical alterations in the entorhinal cortex (EC). We also investigated the possible EC involvement of brain nerve growth factor (NGF), the first neurotrophin to be isolated, during such pathological events. To test this hypothesis, we used pregnant mice exposed to ethanol during EC neurogenesis (starting about gestational day 8). Our data show that prenatal alcohol intake in male mice alters the EC neuronal growth and differentiation. These morphological alterations are accompanied by an altered NGF level in the EC of prenatal alcohol-treated mice. We also found a decrease in choline acetyltransferase- and neuropeptide Y-immunopositive neurons in the EC of alcohol-exposed mice. However, the relationship between neuronal damage induced in the EC by ethanol, low presence of NGF, and the possible functional and behavioral consequences remains to be elucidated.

Animals↗