Search PubMed⌕ Search

Biomedical subjects

M Trabucchi

Publications and source records attributed to M Trabucchi.

At least 307 records · Page 17Linked to original sources
PubMed1983

Ethanol and dopaminergic systems.

Chronic ethanol consumption produces derangements of cell membrane structure, perhaps by changing membrane lipid content. This impairment leads to modification of membrane-related processes. In fact, after chronic ethanol exposure, an increase in striatal adenylate-cyclase activity occurs. On the other hand, dopamine is unable to further potentiate the production of cyclic AMP. This finding demonstrates that the dopaminergic receptor associated with adenylate-cyclase activity is affected by chronic ethanol treatment. In particular, the affinity of the dopaminergic receptor labelled by 3H-Spiperone is enhanced. In addition, the receptor-adenylate cyclase coupling system is impaired after chronic in vivo exposure of animals to ethanol.

Adenylyl Cyclases↗
PubMed1983

Effects of ethanol, given during pregnancy, on the offspring dopaminergic system.

The fetal alcohol syndrome is characterized by a number of abnormalities consisting of a pre- and post-natal growth deficiency, microcephaly, areas of abnormal nerve cell migration in the brain, mental and psychomotor retardation in children of alcoholic women. These findings may be referred as a teratogenic effect of ethanol on the central nervous system. In order to investigate the above ethanol-neurotoxic effect the striatal dopaminergic transmission was studied. The dopaminergic turnover was measured by 3,4-dihyroxyphenilacetic acid content and 3H-Spiperone binding has been carried out to determine dopaminergic receptor alterations induced by chronic ethanol consumption during pregnancy. Our work demonstrates long-lasting modifications of dopaminergic neuronal function after exposure of the experimental animal to ethanol during fetal life. In particular, a decreased receptor function has been observed in rats exposed to ethanol only during the perinatal period. In the same group of rats, diminished receptor activity leads to an enhancement in DOPAC content still detectable after a long period from cessation of ethanol treatment. Neurochemical data are reinforced by behavioral observations. In fact, a significant decrease of spontaneous locomotor activity in the rats chronically treated with ethanol during fetal life was observed. In addition, the altered response of locomotor activity after drug administration may be ascribed to the modified dopaminergic function. With this experimental approach we assume that the action of ethanol on the central nervous system may be a marker of its teratogenic effect.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Decreased content of met-enkephalin-like peptides in superior cervical and coeliac ganglia of aged rats.

Enkephalin like peptides seem to have an important regulatory role at ganglia level. The aim of the present study is to investigate whether the content of enkephalin-like peptides in sympathetic ganglia is affected by the aging process. The results show that the enkephalin like peptides content is low in superior cervical and coeliac ganglia of aged rats (25 months). The age-related decrease of enkephalin content in these structures may be of importance in determining an altered sympathetic control during aging.

Age Factors↗
PubMed1983

Effect of suloctidil on dopaminergic transmission in various rat brain areas: possible uses as drug for the elderly.

Suloctidil is a drug used in the elderly endowed with a mechanism of action at neuronal level which has not been completely explored. The results of the present study indicate that acute treatment with suloctidil induces a decrease of serum prolactin levels and a decrease of 3,4-diidroxyphenylacetic acid concentrations in various rat brain areas. In addition, the repeated injection of small Suloctidil doses produces a down-regulation of dopaminergic receptors. These data suggest that Suloctidil has dopamino-mimetic properties in vivo. This pharmacological activity may be of importance in the clinical action of Suloctidil in the elderly.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Characterization of stereospecific binding of 3H-(-) sulpiride, a selective antagonist at dopamine-D2 receptors, in rat CNS.

Sulpiride endowed with dopamine (DA)-antagonist properties, does not antagonize neostriatal DA-sensitive adenylyl cyclase activity either in vitro or in vivo. Sulpiride however is able to displace radioactive ligands, which label DA-receptors, from their specific binding sites. On these bases sulpiride has been proposed as a selective antagonist at dopamine-D2 receptors. We have characterized 3H(-) sulpiride stereospecific binding in various rat brain areas. In particular, 3H(-) sulpiride binding was found to be saturable, stereospecific and maximally enriched in the synaptic membrane fraction prepared from dopaminergic brain areas. Among a variety of compound tested only DA, DA-agonists and DA-antagonists were competitors for 3H(-) sulpiride specific binding sites. The results suggest that 3H(-) sulpiride may be an useful tool for the characterization and localization of dopamine D2-receptors.

Animals↗
PubMed1983

Changes of beta-endorphin and Met-enkephalin content in the hypothalamus-pituitary axis induced by aging.

The amounts of beta-endorphin- and Met-enkephalin-immunoreactive material are higher in the pituitary of aged rats. However, the aging process decreases the content of beta-endorphin-, but does not affect that of Met-enkephalin-immunoreactive material, in hypothalamus. Thus, it seems that the regulatory mechanisms in the two areas are differentially affected by increasing age. On the other hand, the pituitary increase of these peptides is in line with the assumption that in the elderly the hormonal response to stress is impaired.

Adrenocorticotropic Hormone↗
PubMed1983

Hypertension reduces the number of beta-adrenergic receptors in rat brain microvessels.

Beta-adrenergic receptor function was measured in cerebral microvessels of spontaneously and DOCA-salt hypertensive rats using 125I-iodohydroxybenzylpindolol (IHYP). Both in genetic and in experimental hypertension, a significant decrease in the number of beta-receptor sites was observed, without receptor affinity changes. These results suggest that alterations of central adrenergic regulation of small vessels may participate in the pathogenetic mechanisms leading to the development of the central hypertensive disease.

Animals↗
PubMed1983

Multiple forms of protein kinase from normal human brain and glioblastoma.

The biochemical characteristics of the protein kinase (PK; adenosine triphosphate-protein phosphotransferase, EC 2.7.1.37) isozymes in subcellular preparations from normal human brain cortex and glioblastoma were investigated after chromatography on diethylaminoethyl cellulose, and the following results have been obtained. Two major isozyme forms, eluted by 50 and 200 mM phosphate buffer, are present in both cytosol and membrane-derived preparations from cerebral cortex. Furthermore, these isozyme forms have properties similar to those referred to as type I and type II cyclic adenosine 3':5'-monophosphate-dependent PK. In these chromatographic isozymes, cyclic adenosine 3';5'-monophosphate is more active in stimulating the basal PK enzyme than is cyclic guanosine 3':5'-monophosphate. In glioblastoma, the PK activity from cytosol and particulate preparations is resolved by diethylaminoethyl cellulose in four peaks. In cytosol, the major portion of the enzyme is eluted with a 300 mM buffer (about 50% of the total basal PK activity) and is cyclic nucleotide dependent. On the contrary, in glioblastoma particulate, the PK enzyme is mainly eluted at 50 and 100 mM buffer; neither of these isozymes is cyclic nucleotide dependent. As for cytosol, only the particulate isozyme eluted at 300 mM buffer is strongly activated by cyclic nucleotides. Finally, in both glioblastoma subcellular preparations, only a type II cyclic adenosine 3':5'-monophosphate-dependent PK is present.

Brain↗
PubMed1982

Effects of GTP and sodium on rat striatal dopamine receptors labeled with lisuride.

[3H]Lisuride binding to rat striatal membranes appeared to be stereospecifically displaced by the dopamine antagonist butaclamol. Sodium increased the number of [3H]lisuride binding sites (Bmax) without changing the dissociation constant (Kd). GTP did not affect [3H]lisuride binding characteristics, either with or without sodium. These results suggest that dopamine receptor sites labeled by lisuride are at least in part sodium-dependent, possibly the D2-receptors not involved in adenylate cyclase stimulation.

Animals↗
PubMed1982

Effect of age on beta-adrenergic receptors on cerebral microvessels.

The responsiveness of beta-adrenergic receptors in cerebral microvessels was studied in aged rats by measuring cAMP formation induced by norepinephrine and [125I]iodohydroxybenzylpindolol binding. The density of beta-receptor sites is reduced by aging in the rat cerebral microvessels. These results suggest that the changes in brain circulation during aging may be at least partially due to a reduction of the beta-adrenergic control of cerebral microvessels.

Aging↗
PubMed1982

Ontogenesis of alpha- and beta-receptors located on cerebral microvessels.

Adrenergic receptors in rat brain microvessels were studied during ontogenesis. Microvessels were prepared by albumin floatation and glass bead filtration techniques from cortices of 10, 20- and 90-day-old rats. The lower level of alpha 1- alpha 2- and beta-receptor sites observed in early life may correlate with the lower capacity of cerebral vascular regulatory mechanism in this period.

Aging↗
PubMed1982

Neuronal mechanisms regulating ethanol effects on the dopaminergic system.

Chronic ethanol consumption induces an increase in striatal 3H-Spiroperidol and 3H(-)Sulpiride specific binding by enhancing the affinity between the different dopaminergic recognition sites and the labelled ligands. Dopamine (DA) receptor supersensitivity is also suggested by the enhanced effect of neuroleptics in inducing hypomotility in rats treated with ethanol. The results, obtained by means of the administration of neuroleptics in comparison to ethanol treated rats, indicate a lack of cross tolerance between ethanol and other drugs acting on the dopaminergic recognition sites. These data suggest that ethanol effects on the dopaminergic system are mediated by events involving other neurotransmitter systems.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Action of ethanol and salsolinol on opiate receptor function.

Ethanol may act at the enkephalinergic receptor level through condensation products such as salsolinol. This fact has been demonstrated by studying the 'in vitro' and 'in vivo' salsolinol interaction on enkephalinergic receptor sites labeled by [3H-Met] enkephalin. The modification induced by chronic ethanol and salsolinol on this neuronal system is a reduction of the affinity of the receptor for its ligand. These data suggest that a down regulation process due to the continuous opiate receptor stimulation occurs after ethanol administration.

Acetaldehyde↗
PubMed1982

Ethanol metabolism and striatal dopamine turnover.

In recent reports it has been indicated that acute and chronic ethanol treatments affect the central dopaminergic system. In particular, after acute ethanol administration it has been detected an increase of dopamine (DA) turnover measured as dihydroxyphenylacetic acid (DOPAC) content in rat corpus striatum. In order to verify the correlation between these neuronal events and the metabolism of ethanol, we measured striatal DA activity after different experimental manipulations of liver function. Ethanol metabolic rate has been stimulated by administering phenobarbital sodium, while liver ethanol metabolism was decreased with a subtotal hepatectomy. In these conditions we found a shift to the left of the time curve for DOPAC levels and a significant reduction of the peak of DOPAC increase respectively. In this paper we report that acetaldehyde induces modifications of the striatal DOPAC content, which become significant after a shorter latency period in comparison with the acute ethanol injection. Our data suggest the hypothesis that the neurochemical effects of ethanol may be mediated by the formation of specific metabolic products.

3,4-Dihydroxyphenylacetic Acid↗