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D Maysinger

Publications and source records attributed to D Maysinger.

At least 73 records · Page 4Linked to original sources
PubMed1990

Evidence for nerve growth factor-ganglioside interaction in forebrain cholinergic neurons.

Cholinergic neurons of the forebrain respond trophically to nerve growth factor (NGF) in some experimental circumstances. The cholinergic cell system of the nucleus basalis magnocellularis (NBM) which projects to the cortex shows signs of cellular degeneration following limited devascularizing cortical lesions, while no apparent damage is observed in the remaining ipsilateral cortex. These cholinergic cells possess receptors for NGF and the administration of this peptide into the cerebroventricular space prevents cell shrinkage and loss of activity of the biosynthetic enzyme for acetylcholine, choline acetyltransferase (ChAT). Analogous trophic responses can be elicited in this system with the application of the sialoganglioside GM1. In addition, GM1 can increase the effects of NGF on ChAT activity in lesioned neurons of the NBM-to-cortex model system described above. This cooperative interaction is observed even when ineffective doses of GM1 are administered. Furthermore, an interaction between these two putative neurotrophic substances has been noted over other cholinergic parameters such as cortical high affinity choline uptake (HACU). These studies confirm the idea that trophic factors can be utilized to rescue degenerating neurons of the CNS and, in addition, lend support to the concept that gangliosides can facilitate actions of endogenously produced trophic factors.

Animals↗
PubMed1989

Effects of microencapsulated monosialoganglioside GM1 on cholinergic neurons.

The preparation, physical characterization and effects of microcapsules containing the monosialoganglioside GM1 in an in vivo rat model are described herewith. Several preparations of microcapsules were obtained differing in physical and chemical properties. Human serum albumin (HSA) microcapsules with or without GM1 are spherical in shape, have a consistent particle size (8-10 microns in diameter) and are devoid of large pores. In agreement with our previous work, we now provide further evidence that GM1 can prevent shrinkage and the decrease of choline acetyltransferase activity in the nucleus basalis magnocellularis (NBM) of the rat following a unilateral cortical lesion. In the present study we examined the effect of microencapsulated GM1 in this in vivo rat model. Local application of HSA-microencapsulated GM1 (in doses comparable to those obtained by i.c.v. administration) onto the surface of the lesioned cortex prevents both the biochemical and morphological degenerative changes in the NBM of rats with unilateral devascularizing cortical lesions. The results from these studies show that microencapsulated GM1 can be applied successfully and a prolonged controlled release of this drug obtained, thus avoiding surgical implantation of a cannula.

Animals↗
PubMed1989

Gangliosides potentiate in vivo and in vitro effects of nerve growth factor on central cholinergic neurons.

The effects of nerve growth factor beta (beta-NGF) and ganglioside GM1 on forebrain cholinergic neurons were examined in vivo and in vitro. Following unilateral decortication of rats, GM1 (5 mg/kg per day) administered intracerebroventricularly could protect forebrain cholinergic neurons of the nucleus basalis magnocellularis from retrograde degeneration in a manner comparable to beta-NGF. Administered in combination with beta-NGF, GM1 produced a significant increase in choline acetyltransferase activity in the nucleus basalis magnocellularis and remaining cortex ipsilateral to the lesion. Concentrations of GM1 that were ineffective when administered alone in this lesion model, when given with beta-NGF, potentiated beta-NGF effects in both of the above brain areas. In dissociated septal cells in vitro, an increase in choline acetyltransferase activity was noted at beta-NGF concentrations as low as 0.1 pM and reached a plateau at 1 nM. A moderate (up to 35%) stimulation of choline acetyltransferase activity was observed with 10 microM GM1. The application of beta-NGF in combination with 10 microM GM1 or 0.1 microM GM1, a concentration that is ineffective in these cultures, produced a much greater increase in choline acetyltransferase activity than did beta-NGF alone. These observations support the idea that exogenously applied gangliosides can elicit trophic responses in cholinergic neurons of the central nervous system. That GM1 increases and even potentiates beta-NGF effects suggests that some of the trophic actions of this compound may be mediated through endogenous trophic factors.

Animals↗
PubMed1988

Striatal and cortical acetylcholine release in vivo in rats with unilateral decortication: effects of treatment with monosialoganglioside GM1.

Striatal and cortical extracellular acetylcholine (ACh) and choline (Ch) levels were determined in samples collected under in vivo conditions using microdialysis in normal (naive) and decorticated rats treated with saline or the monoganglioside GM1. ACh and Ch were assayed using a sensitive high performance liquid chromatography technique coupled to a postcolumn reactor with immobilized enzymes. Picomole amounts of ACh could be measured in the presence of an acetylcholinesterase inhibitor (neostigmine) in the microdialysis perfusion medium (striatal ACh = 0.2-0.4 microM; cortical ACh = 0.03-0.04 microM). Ch was detected both in the presence and in the absence of neostigmine (striatal Ch = 0.5-0.6 microM; cortical Ch = 0.6-2 microM). ACh, but not Ch, was strongly stimulated by 100 mM of KCl included in the perfusion medium. Decortication produced by devascularization did not significantly modify the cortical or striatal basal levels of ACh. However, in the cortex, KCl produced a higher ACh stimulation in the GM1-treated than in the saline-treated decorticated or naive rats. The present results indicate that GM1-treatment increases the ability of cortical cholinergic terminals to release ACh and support the idea that trophic factors such as monoganglioside GM1 can promote recovery following injuries of the central nervous system.

Acetylcholine↗
PubMed1987

Neural plasticity of basal forebrain cholinergic neurons: effects of gangliosides.

Nucleus basalis magnocellularis (NBM) cholinergic neurons, furnishing the major portion of the extrinsic cholinergic innervation of the rat cortex, undergo specific retrograde changes in cell somata and choline acetyltransferase (ChAT) activity after cortical lesions. These are prevented in young and mature animals, but not in aged rats, by the chronic administration of exogenous ganglioside GM1 after lesioning. However, a delay of 10 days (in young animals) in the commencement of treatment averted the responses to GM1 in lesioned animals. It is suggested that the effects of exogenous gangliosides on retrograde biochemical and morphological alteration of cholinergic neurons may vary with circumstances permissive of plastic changes of central nervous system neurons at the time of administration.

Animals↗
PubMed1986

Cholinergic and GABAergic neurotoxicity of some alkylating agents.

A series of nitrogen mustard derivatives was tested for neurotoxic effects on cholinergic and GABAergic markers at three rat brain regions: hippocampus, striatum and cortex. All compounds were administered intracerebroventricularly, and the enzymatic activities were measured 7 days after treatment. The effects of synthesised nitrogen mustard derivatives with indole, quinoline and hemicholinium backbone structures were compared. Of these compounds, only the hemicholinium analogue showed some preferential neurotoxicity to cholinergic neurones, thus offering a basis for designing novel, more specific cholinergic neurotoxins.

Alkylating Agents↗
PubMed1986

Hemicholinium mustard derivatives: preliminary assessment of cholinergic neurotoxicity.

We have attempted to design novel neurotoxins based on the use of hemicholinium derivatives. Three compounds were tested for their neurochemical effects on cholinergic, gabaergic and catecholaminergic markers in the hippocampus, striatum and cortex following intracerebroventricular administration. The effects were compared with those of the non-specific alkylating agent (nitrogen mustard) and the previously reported ethylcholine mustard aziridinium ion (AF 64A). The results indicate that only one of these derivatives (HcM-9) exhibits comparable neurotoxic effects on cholinergic markers with a similar pattern of specificity to that of AF 64A. In addition, HcM-9 showed less overall toxicity, this being reflected in a higher survival rate. The present results indicate that hemicholinium derivatives could be good substrates for further molecular modifications, thus a step towards the design of a more specific cholinergic neurotoxin.

Animals↗
PubMed1985

Flavonoid content in propolis extracts and growth inhibition of Bacillus subtilis.

Thirty eight propolis samples were collected in several regions of SR Croatia differing in climate and vegetation. Amounts of 3,5,7-trihydroxyflavone and of 5,7-dihydroxyflavonone were determined chromatographically in individual propolis samples. Concentrations of each constituent were correlated with the growth inhibitions of Bacillus subtilis (IP-5832).

Bacillus subtilis↗
PubMed1984

Differential effects of various opioid peptides on vasopressin and oxytocin release from the rat pituitary in vitro.

Dynorphin (1-17), and to a lesser extent, beta-endorphin and [Leu]enkephalin (10(-6) M each) decreased the spontaneous release of vasopressin (VP) from the rat neurointermediate pituitary in vitro, whereas the oxytocin (OT) release remained unchanged. Naloxone, however, did not significantly alter the spontaneous VP and OT release. Dynorphin (1-17) (10(-7) M) increased the electrically evoked release of VP and OT, while 10(-6) M had a significant, somewhat less pronounced stimulatory effect only on VP, but not on OT release. The opiate inactive fragment [des-Tyr1]dynorphin (1-17) did not change the evoked VP and OT release, indicating that the dynorphin effect was mediated by opiate receptors. beta-Endorphin (10(-6) M and 10(-7) M) did not alter the evoked VP and OT secretion. 10(-6) M [Leu]enkephalin induced a stimulation of the evoked OT, but not VP release; 10(-7) M [Leu]enkephalin had no effect, neither on VP nor on OT release. The opiate antagonist naloxone (10(-5) M) induced an increase in the evoked VP and, even more pronounced, OT release. In a concentration of 10(-6) M, however, naloxone only increased the evoked OT release. When naloxone and dynorphin (1-17) were concomitantly applied, their stimulatory effects on the evoked VP and OT release were additive. Similarly to the effects of naloxone, addition of a monoclonal antibody which binds to the common N-terminal sequence of all endogenous opioid peptides, resulted in a marked increase in the evoked secretion of VP and, to an even more pronounced degree, of OT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Differential effects of acute and chronic ethanol treatment on particular opioid peptide systems in discrete regions of rat brain and pituitary.

Acute ethanol treatment induced a significant increase in the tissue levels of immunoreactive (ir-) Met-enkephalin in hypothalamus, striatum and midbrain, but not in hippocampus. Levels of ir-dynorphin, ir-alpha-neo-endorphin and ir-beta-endorphin were not found to be significantly altered in brain and pituitary. Chronic ethanol treatment (by the use of ethanol liquid diet) resulted in a more than 50% decrease of the tissue levels of ir-dynorphin and ir-alpha-neo-endorphin in hypothalamus and hippocampus, while both peptides remained unchanged in midbrain, striatum, adenohypophysis and neurointermediate pituitary. In contrast, ir-met-enkephalin was decreased in striatum and hypothalamus, but unaffected in midbrain and hippocampus. Levels or ir-beta-endorphin remained unchanged in the brain and in the pituitary. However, the de novo biosynthesis of beta-endorphin and its prohormones beta-lipotropin and pro-opiomelanocortin was increased in the intermediate pituitary and to an even more pronounced degree, in the adenohypophysis, after chronic treatment of rats with ethanol liquid diet, nevertheless, the amounts of opiate-active beta-endorphin were found to be reduced in both lobes of the pituitary: In the adenohypophysis, this was due to a retardation of the enzymatic processing of beta-endorphin from its precursor beta-lipotropin, while in the intermediate pituitary the alpha-N-acetylation of beta-endorphin to opiate-inactive alpha-N-acetyl-beta-endorphin was stimulated. In conclusion, acute and chronic ethanol treatment caused selective alterations on different opioid peptide systems within distinct areas of the rat brain and pituitary.

Acetylation↗
PubMed1982

Growth inhibition of bacillus subtilis and composition of various propolis extracts.

The composition of 31 samples of propolis extract was investigated by using TLC. Ethanol extract of propolis (EEP) prepared from the various propolis samples differ mainly in quantities of identified compounds, and not in kind of components present. According to the inhibitory activity against Bacillus subtilis, the propolis samples were grouped in three categories. It appears that the galangin content in a sample is a main constituent, which determines its antibacterial activity.

Anti-Bacterial Agents↗
PubMed1982

Inhibition of growth and biosynthesis of ochratoxin A in Aspergillus sulphureus NRRL 4077 by propolis extract.

Growth inhibition of Aspergillus sulphureus NRRL 4077 and biosynthesis of ochratoxin A in the presence of propolis was investigated. Although the growth of the micro-organism was inhibited at all concentrations of applied propolis extract up to d 10 of incubation, only the 2.0 mg/ml concentration of propolis exhibited definite fungistatic activity. Ochratoxin A was detected in all culture media, but its amounts were low in the first 10 d of experiment. In comparison with the control culture, the amounts of ochratoxin A were proportional to the growth of A. sulphureus and reciprocal to the amounts of propolis extract used.

Aspergillus↗
PubMed1981

Binding (in vitro) of some antimitotic isatin derivatives to human serum albumin.

The binding of isatin and its mustard N-Mannich base, considerably biologically active compounds, to human serum albumin has been studied by equilibrium dialysis and ultrafiltration. The influences of ligand and macromolecule concentration, temperature and pH of the incubation medium have been demonstrated. The Scatchard plot of isatin binding to albumin shows a biphasic curve which indicates the presence of at least two different binding sites on albumin molecule. One site with a higher affinity, K1 = 2.25 X 10(3) M and n1= 25, and the other site with a lower affinity, i.e. higher capacity. In the cases of mustard Mannich base we could demonstrate the same type of curve, K1 = 2.20 X 10(5) M and n1 = 1.0, whereas another site has a lower affinity and greater number of binding sites.

Humans↗