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L Aloe

Publications and source records attributed to L Aloe.

At least 181 records · Page 10Linked to original sources
PubMed1992

[Randomized study on the use of propofol for anesthesia in intracranial tumors. Comparison with balanced anesthesia].

There is currently no anesthesiological technique which enables volume, cerebral blood flow and spinal fluid pressure to be kept constant. The aim of the present study was to compare two techniques of anesthesia in patients with cerebral tumours: one of a balanced type (AB) and the other of a continuous ev type (AEC) using propofol in order to assess which guaranteed the greatest cerebral protection. The results of the study have shown that the use of propofol may represent a useful alternative in intracranial tumour surgery since changes in systolic pressure and heart rate observed during AEC anesthesia were statistically lower in comparison to AB anesthesia. No statistically significant differences were observed in relation to changes in diastolic pressure, PVC, ApCO2 and the incidence of bleeding or cerebral edema. The quality of awakening was better in patients in the AEC group in terms of renewed breathing and spontaneous motility, verbal response and space-time orientation.

Adult↗
PubMed1992

Cellular localization of nerve growth factor-like immunoreactivity in hippocampus and septum of adult rat brain.

The cellular localization of the nerve growth factor-like immunoreactivity (NGF-LIR) has been studied in the intact adult rat brain at the level of the hippocampus and the septum. Immunolabelling for NGF combined with counterstaining with cresyl violet and double immunostaining technique, which allowed simultaneous localization of NGF-LIR and that of astroglial marker -GFAP, were used. The data indicate neuronal localization of NGF-like immunoreactivity and a lack of colocalization of NGF-LIR with the immunoreactivity of GFAP in the hippocampus. These data are consistent with in situ hybridization results for NGF and immunocytochemical results for pro-NGF localization obtained by others. At the septal level, apart from neuronal localization of NGF-LIR, single NGF-like immunoreactive astrocytes have been observed. This suggests that, although to a very small extent, in vivo intact brain astrocytes may, just as astrocytes growing in vitro, synthesize NGF-like molecules. This finding may be of importance in better understanding the trophic support for NGF responsive cholinergic neurones in the brain.

Animals↗
PubMed1991

Capsaicin affects aggressive behavior, but not hot plate responding, of adult male mice.

Adult male mice of albino Swiss-derived CD-1 strain were used to assess the effects of capsaicin (a powerful agent that produces a marked depletion of the undecapeptide substance P) on both intraspecific aggressive behavior (induced by 8 weeks of individual housing) and pain sensitivity. Capsaicin was given SC, 48 h before behavioral testing. Aggressive behavior, scored during a 5-min session under red light, was significantly enhanced by capsaicin treatment (50 or 100 microliters of a 7.5 mg/ml solution). In fact, Total Aggressive Episodes, Attacks, and Upright Offensive Posture were significantly higher in the two capsaicin-treated groups, while Latency to the first Attack was decreased, when compared to both vehicle or unhandled controls. A concomitant decrease in Submissive Postures and Flee was also evident in capsaicin mice. Hot plate testing (55 +/- 0.1 degrees C, cutoff time 30 s), carried out on nonisolated mice, did not reveal any difference among the two capsaicin groups (same doses) and vehicle or unhandled controls.

Aggression↗
PubMed1991

Effect of acetyl-L-carnitine on forebrain cholinergic neurons of developing rats.

It has been shown that the endogenous compound, acetyl-L-carnitine (ALCAR), acts in the brain as a metabolic cofactor in the synthesis of acetylcholine. In these studies, ALCAR was injected into the brain of developing rats every other day for the first three weeks after birth in order to assess its effect on forebrain cholinergic neurons. The results showed that intracerebroventricular (icv) administration of ALCAR causes an increase of choline acetyltransferase (ChAT) activity and of nerve growth factor receptor expression in the striatum. Biological assays of brain tissues revealed that the level of nerve growth factor (NGF) in the hippocampus also increases. The ability of brain cholinergic tissues to respond to exogenous administration of ALCAR is discussed.

Acetylcarnitine↗
PubMed1991

In vivo and in vitro effect of NGF on bursa of Fabricius cells during chick embryo development.

NGF exerts a broader biological action than previously believed. The growing-evidence of NGF's effect on lymphocytes and the presence of high levels of mRNA for NGF receptors in the embryonic bursa of Fabricius led us to study the action of NGF on bursal cells during chick embryo development. Our in vivo experiments indicate that NGF administration in ovo caused a significant increase in size of the lymphoid follicles in the embryonic bursa at E15. The in vitro experiments demonstrated that NGF exhibits different effects on bursal cells depending on the stage of development. At E9 bursal cells survive for longer periods when NGF is added to the medium. At E15 NGF act as a colony-stimulating factor by significantly increasing the number of colonies in soft agar cultures.

Animals↗
PubMed1990

Changes of NGF level in mouse hypothalamus following intermale aggressive behaviour: biological and immunohistochemical evidence.

Nerve growth factor (NGF) immunoreactivity was detected in the hypothalamus of adult male mice. NGF-immunoreactive cell bodies were examined through consecutive brain sections, and it was found that most of the NGF-positive cells were located in the dorsomedial and mediolateral portions of the hypothalamus. Tissue culture bioassays showed that hypothalamic extract elicits neurite outgrowth from both chick sensory ganglia and rat superior cervical ganglia neurons, and that these effects are inhibited by addition of NGF antibodies. Our results also showed that intermale aggressive behaviour induced by 6-8 weeks of social isolation induces an NGF increase in the hypothalamic area, which is not abolished by sialoadenectomy, suggesting that the increased brain NGF is locally synthesized, and does not come from salivary sources. Likewise, the level of NGF in the hypothalamus of adrenalectomized fighting mice increased, although to a much lesser extent, when compared to hypothalamic levels of sham-operated fighting mice. The present results and a recent report showing that aggressive behaviour causes an increase of mRNANGF in hypothalamic areas are discussed in relation to a possible functional role of NGF in these brain structures.

Aggression↗
PubMed1990

Social status and nerve growth factor serum levels after agonistic encounters in mice.

Ten repeated daily interactions (20 min each) of the same pairs of isolated male mice produced a clear distinction between attacking (dominant) and defeated (subordinate) animals. The fighting level remained fairly constant over the 10 days. One hr after the end of the 10th session, the increase in serum NGF levels described previously (2) was significantly more marked in subordinate than in dominant mice. The mean level of serum NGF was correlated with the number of fighting episodes, particularly in the case of dominant individuals. Moreover, within-pair differences in NGF values were correlated with differences in locomotor activity between dominants and subordinates; this makes it possible that stimuli other than those produced by fighting per se may be responsible for the increase in circulating NGF. As is well known, the adrenal hypertrophy produced by fighting stress is more marked in subordinate than in dominant mice, while previous work has shown that stress of a nonpsychosocial kind does not elevate serum NGF levels. Therefore, the present data support the hypothesis that NGF release contributes to the modulation of adrenal function in a situation-specific fashion.

Aggression↗
PubMed1990

Nerve growth factor released into the bloodstream following intraspecific fighting induces mast cell degranulation in adult male mice.

Nerve growth factor (NGF) is stored in the salivary glands of adult male mice. Recent evidence has shown that NGF is active on cell lines of the immune system. Following isolation-induced fighting (20 min session) NGF is released into the bloodstream, causing disruption of cytoplasmic membranes and concomitant degranulation of peritoneal mast cells (MCs). Fluorometric determinations showed an increase in histamine levels in the peritoneal fluid of fighting mice. Administration of NGF antibodies or sialoadenectomy prior to the fighting session blocks MC degranulation. These results, together with other observations, suggest that endogenous NGF plays a physiological role in MC activation.

Aggression↗
PubMed1990

Effect of adrenal gland hormones on NGF level and choline acetyltransferase activity in rat brain.

The effect of adrenal gland hormones on brain NGF-producing cells and on NGF target cells was studied in young adult rats. The results showed that adrenalectomy causes a decrease in the NGF level in the hippocampus and of choline acetyltransferase in the septum. These studies suggest that adrenal gland hormones are involved in the regulation of NGF in specific brain structures.

Adrenalectomy↗
PubMed1989

NGF primed spleen cells injected in brain of developing rats differentiate into mast cells.

The aim of this work was to study the topographic distribution and the morphological behaviour of nerve growth factor (NGF) primed spleen cells injected into the lateral ventricles of developing rat brain. Serial coronal brain sections showed that these transplanted cells acquire phenotypical characteristics similar to those of mast cells (MCs) and that they enhance local neovascularization. These results, together with the observation that these cells are located in proximity to the hippocampus, a brain tissue which contains one of the highest levels of NGF, provide a model for studying the relationship between NGF and MC differentiation and secretion.

Animals↗
PubMed1989

Adrenalectomy decreases nerve growth factor in young adult rat hippocampus.

The effect of adrenalectomy on the level of nerve growth factor (NGF) in the hippocampus and on the distribution of choline acetyltransferase immunoreactivity in forebrain cholinergic neurons of developing rats was studied. Biological and immunohistochemical determinations indicated that in 40-day-old rats, adrenalectomy reduced the NGF level in the hippocampus and the choline acetyltransferase immunoreactivity in the septal lateral bands. Furthermore, autoradiographic studies showed that adrenalectomy causes changes in the distribution and expression of NGF receptors in the hippocampus. These results suggest that adrenal hormones are involved in the regulation of the NGF level in the hippocampus and of NGF receptors in the septum.

Adrenalectomy↗
PubMed1989

Nerve growth factor mRNA and protein increase in hypothalamus in a mouse model of aggression.

The effects of intermale aggressive behavior induced by social isolation on the level of nerve growth factor (NGF) mRNA and protein were investigated in central and peripheral mouse tissues. A large increase in NGF mRNA and protein was observed in hypothalamus, with no changes in cerebral cortex, hippocampus, and cerebellum. No change in NGF mRNA levels was found in heart, spleen, vas deferens, and submaxillary salivary gland. The cellular localization of NGF mRNA in the central nervous system was investigated by in situ hybridization. Numerous nerve cells were specifically labeled in preoptic and ventrolateral nuclei of the hypothalamus, as well as in the cornu ammonis region of the hippocampus and throughout all layers of the cerebral cortex, with the highest concentration in layer III. The present results firmly establish that nerve cells constitute the major source in NGF in the brain. They also open the way to understanding the regulation of NGF biosynthesis in the central nervous system.

Aggression↗
PubMed1988

The effect of nerve growth factor and its antibody on mast cells in vivo.

Repeated subcutaneous administration of nerve growth factor (NGF) into newborn rats caused an increase in number and size of free and tissue-adherent mast cells (MCs). In vivo and in vitro autoradiographic studies show that MCs exhibit specific binding sites for NGF. Peritoneal MCs of adult rats exposed to high titers of endogenous (autoimmunization) and exogenous NGF antibodies showed severe cytological alterations and decreased in number. Light and electron microscopic studies revealed that MC destruction took place slowly (7-10 days) and required continual exposure to high titers of NGF antibodies. The role played by NGF in the hematopoietic cell lineage is at present under study in our laboratory.

Age Factors↗
PubMed1987

Intraocular herpes simplex virus injection in neonatal rats induces sympathetic nerve cell destruction: effect of nerve growth factor.

The effect of herpes simplex virus (HSV) injection on the sympathetic nerve system of newborn rats was studied at structural, ultrastructural, and immunohistochemical levels. It was found that HSV injected into the anterior eye chamber is retrogradely transported and reaches the nerve cell bodies of the ipsilateral superior cervical ganglion (SCG) after 18-24 hr, causing complete cell destruction within 3-4 days. In subsequent days, nerve cells of the contralateral SCG, spinal sensory ganglia, chromaffin cells and brain cells also become infected and are eventually killed by the virus. Pretreatment with nerve growth factor (NGF) produces an initial protection from viral cell destruction, but does not block the final, lethal effect of the virus. These investigations demonstrate that sympathetic nerve cell destruction can be induced in newborn rodents by HSV, and that NGF treatment renders the cells, for a time-limited period, more resistant to the virus.

Adrenergic Fibers↗
PubMed1986

Pretreatment of young mice with nerve growth factor enhances scopolamine-induced hyperactivity.

Twenty-one-day-old mice show a characteristic enhancement of locomotor activity upon injection of the cholinergic (muscarinic) blocking drug scopolamine. Intracerebral (third ventricle) injection of nerve growth factor (NGF) 24 h prior to scopolamine injection significantly enhances the drug-induced hyperactivity without modifying baseline activity. Such potentiation of the scopolamine effect was not obtained in 10-week-old mice treated and tested similarly.

Age Factors↗
PubMed1986

Aggressive behavior induces release of nerve growth factor from mouse salivary gland into the bloodstream.

Intraspecific fighting induced by 6-8 weeks of social isolation results in massive release of nerve growth factor (NGF) into the bloodstream of adult male mice. The amount of circulating NGF is highly correlated with the number of fighting episodes. Biological, radioimmunological, immunohistochemical, and ultrastructural studies show that NGF is discharged from the salivary gland into the blood within minutes after fighting and reaches the highest level 3-4 hr later. Adrenergic innervation of the salivary gland or adrenalectomy does not abolish the NGF release. Corticotropic hormones do not induce NGF increase in the blood. Daily administrations of highly purified NGF (3 micrograms per g of body weight) result in a considerable increase in the volume of adrenal glands. These findings are unequivocable evidence for a physiological role of the mouse salivary glands as a major source of blood NGF.

Adrenalectomy↗