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Biomedical subjects

M Trabucchi

Publications and source records attributed to M Trabucchi.

At least 253 records · Page 14Linked to original sources
PubMed1987

Microcirculation and neurotransmitter metabolism in the pathophysiology of brain ischaemia. A role for calcium.

Calcium is an essential component in a multitude of cellular processes, ranging from muscle contraction to cell division, and hormone and neurotransmitter release. Disruption of calcium homeostasis at the neuronal level, which occurs in pathological events such as ischaemia, causes a series of biological reactions that ultimately lead to cell death. Furthermore, calcium-triggered events may influence vascular activity, causing spasm at the level of the major vessels and inducing changes in the permeability of the blood-brain barrier. Thus, knowledge of the biochemical events involved in the initiation and progression of cell injury occurring in acute cerebrovascular events may have important implications for possible strategies of pharmacological intervention such as calcium entry blockade.

Blood-Brain Barrier↗
PubMed1987

In vitro and in vivo effect of ethanol on cyclic AMP dependent protein phosphorylation.

The in vitro addition of ethanol reduces the cyclic AMP dependent protein phosphorylation of several protein bands both in particulate and in cytosolic fractions of rat striatum. The cytosolic 32 Kd band associated to D-1 dopamine receptor is particularly sensible to the inhibitory action of ethanol. In vivo data indicate that chronic ethanol treatment exerts also an inhibitory effect on protein phosphorylation in striatal fractions reducing the 32P incorporation in protein bands linked to the synaptic vescicular traffic and to dopaminergic transmission. This study provides direct evidence that long term ethanol consumption alters dopaminergic transduction processes.

Animals↗
PubMed1987

Heavy drinking decreases plasma met-enkephalin concentrations.

Plasma met-enkephalin immunoreactive material (ME-IR) concentration was measured in 175 aged subjects (68 males, 107 females). Heavy drinking (1 liter of red or white wine a day, equivalent roughly to greater than 110 g ethanol) was associated with reduced ME-IR concentrations. On the other hand, no correlation was found between plasma ME-IR and other parameters such as blood pressure, age or body weight. These data favor the hypothesis of an involvement of ME-IR in the mechanisms of ethanol action.

Aged↗
PubMed1986

Release of met-enkephalin from rat striatal slices: effect of amphetamine and fipexide.

The release of Met-enkephalin immunoreactive material (ME-IR) from rat striatal slices is affected by exposure to amphetamine and fipexide (chloro-4-phenoxy)-2-acetyl-1-(methylene-dioxy 3, 4-benzyl-4-piperazine) a psychostimulant drug with mild dopaminomimetic activity. Both amphetamine and fipexide inhibited in vitro the release of ME-IR. The same effect was observed after in vivo acute administration and is also maintained after chronic treatment. The action of fipexide and amphetamine is still present after reserpine pretreatment. The results indicate that fipexide may facilitate dopamine neurotransmission by inhibition of an enkephalinergic inhibitory feed-back circuit.

Amphetamines↗
PubMed1986

Effect of lead exposure on dopaminergic receptors in rat striatum and nucleus accumbens.

Haloperidol- and sulpiride-displaceable [3H]spiroperidol binding and the dopamine-inhibited adenylate cyclase were measured in rats chronically exposed to lead acetate. Haloperidol-displaceable [3H]spiroperidol binding was unmodified while sulpiride-displaceable binding was increased in striatum and decreased in nucleus accumbens. In addition, the decrease of sulpiride-displaceable binding in nucleus accumbens was paralleled by a reduced ability of bromocriptine to inhibit cAMP formation in presence of the D1 receptor antagonist SCH 23390. The results support the concept that in vivo lead treatment affects dopaminergic receptors and that the binding sites labelled by [3H]spiroperidol displaced by haloperidol may be different from those which recognize sulpiride.

Adenylyl Cyclases↗
PubMed1986

[Vascular and neuronal mechanisms of calcium antagonists. Significance in neurological therapy].

Calcium-channel entry blockers are drugs with different chemical properties and a common pharmacological characteristic. Calcium is very important in many physiological mechanisms and could be involved in neuronal damage following cerebral ischemia. Thus, calcium-channel blockers agents could be of interest in medical treatment of cerebrovascular diseases, headache and subarachnoid hemorrhage. Calcium-channel blockers seem to have a direct protective role against neuronal ischemic damage and/or a direct action on cerebral vessels. Some clinical experiences have suggested a protective role of nimodipine in the prevention of ischemic complications related to cerebral vasospasm after subarachnoid hemorrhage.

Blood-Brain Barrier↗
PubMed1986

Cyclic AMP-dependent protein phosphorylation is reduced in rat striatum after chronic ethanol treatment.

Endogenous protein phosphorylation by cyclic AMP-dependent protein kinase was found reduced in striatal membranes obtained from chronic ethanol-treated rats. Experiments using an exogenous substrate show that the decreased response is due to a deficiency in the phosphorylating activity of the cyclic AMP-dependent protein kinase and not to a lack of endogenous substrate for phosphorylation.

Alcoholism↗
PubMed1986

Neurotensin effect on dopamine release and calcium transport in rat striatum: interactions with diphenylalkylamine calcium antagonists.

The release of dopamine was investigated in rat striatal slices exposed in vitro to neurotensin. This peptide increased basal and K+-evoked dopamine release. Moreover neurotensin antagonized the flunarizine-induced inhibition of K+-stimulated dopamine release. The K+-evoked 45Ca2+ accumulation was also inhibited by flunarizine. This effect was antagonized by neurotensin. The results suggest that dopamine release in rat striatum is regulated by different molecular events also of peptidergic nature having as possible mechanism of action an influence on calcium ion movements.

Animals↗
PubMed1986

Regional modification of brain calcium antagonist binding after in vivo chronic lead exposure.

Lead toxicity in the central nervous system seems to be partially related to specific effects of the metal on calcium metabolism and in particular on calcium transport. On this line, the present study investigates the characteristics of [3H]nitrendipine binding to several rat brain regions after in vitro lead addition or after in vivo chronic exposure to this metal. In vivo a lead induced increase in [3H]nitrendipine binding, Bmax, is observed in cerebral cortex and striatum while the binding is unmodified in hippocampus. The in vitro studies are in agreement with in vivo data; lead addition stimulates the binding in synaptic membranes prepared from cortex and striatum but not from hippocampus where the binding is slightly inhibited. The data suggest that lead interferes with neuronal calcium channels in an area-selective manner.

Animals↗
PubMed1986

Chronic lead exposure alters dopaminergic mechanisms in rat pituitary.

The effect of chronic lead treatment on pituitary dopamine (DA) D2 receptors was studied by measuring (-)sulpiride-displaceable [3H]spiroperidol-binding and DA-inhibited adenylate cyclase. Receptor number was reduced in lead-exposed animals and bromocriptine was less able to inhibit cyclase activity in pituitary homogenates. In addition, the capacity of DA to inhibit the VIP-stimulated cAMP formation was decreased.

Adenylyl Cyclase Inhibitors↗
PubMed1986

Age-related changes in neurotensin content and receptors in various rat brain areas.

Neurotensin immunoreactivity (NT-IR) is significantly reduced in striatum, nucleus accumbens and hippocampus but not in frontal cortex, hypothalamus and septum of 24-month-old male Sprague Dawley rats. Neurotensin binding in cortex, striatum, hypothalamus and hippocampus shows a rather uniform decline with age. The changes in NT-IR content in striatum and nucleus accumbens are of particular interest in view of the existence of a functional relationship between dopamine and neurotensin.

Aging↗
PubMed1986

Different patterns of CSF neurotransmitter metabolism in patients with left or right hemispheric stroke.

In 30 ischemic stroke patients, divided into 2 groups depending on the side of their hemispheric cerebral lesion, the authors evaluated the levels of CSF homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). The changes of these metabolites in CSF samples collected 3, 14 and 25 days after stroke have been correlated to the clinical course. In both groups, which were similar in respect to the localization of the infarcted area and to the volume of the lesion, the levels of HVA and 5-HIAA increased in the first 2-3 days and gradually declined to normal values in the following 3 weeks, in parallel with the regression of neurological deficits. The increase of HVA and 5-HIAA was statistically significant only in left hemisphere-injured patients. A linear regression analysis between the clinical score values and the CSF levels of the two metabolites at different time-points of observation revealed a significant correlation only for the HVA in the left-lesioned patients.

Aged↗
PubMed1986

Partial reversal of asymmetry in microvessel neurochemical changes after ischemia by corpus callosum section.

Common carotid occlusion in the rat significantly decreases the density of beta-adrenergic receptors in preparations of microvessels obtained from ipsilateral and contralateral cerebral cortices. The disruption of nerve pathways connecting the hemispheres (callosal transection) partially reverses the effect of common carotid occlusion on beta-adrenergic receptor density in capillaries of the contralateral cortex. In addition, the destruction of the central noradrenergic system by intraventricular injection of 6-hydroxydopamine abolishes the effect of ischemia on capillary beta-adrenergic receptor function in both hemispheres. The results suggest that beta-adrenergic receptors located on microvessels are partially regulated by neuronal pathways and that focal ischemia induces neurochemical and functional changes in remote areas of the brain.

Animals↗
PubMed1986

Changes in the interaction between CNS cholinergic and dopaminergic neurons induced by L-alpha-glycerylphosphorylcholine, a cholinomimetic drug.

The present study investigates the cholinomimetic properties of the drug L-alpha-glycerylphosphorylcholine (alpha-GPC) at CNS level. Experiments using tritium labelled alpha-GPC indicate that the drug reaches the brain after i.p. and per os administration. In order to study the cholinomimetic properties of this drug an indirect functional index of cholinergic activation was used. In fact cholinergic agonists induce an activation of striatal dopaminergic output. alpha-GPC both i.p. and per os administered increased striatal dihydroxyphenylacetic acid (DOPAC) content. In addition, the in vitro K+ stimulated dopamine release was increased in rats treated in vivo with alpha-GPC. Since alpha-GPC has a weak displacing activity in QNB binding, the in vivo cholinergic activity might be due to the fact that this drug may increase the availability of choline for acetylcholine synthesis leading to increased acetylcholine production. This activity may be useful in those situations such as aging in which cholinergic activity is deficient.

Animals↗