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Biomedical subjects

S Govoni

Publications and source records attributed to S Govoni.

At least 127 records · Page 7Linked to original sources
PubMed1987

Erythrocyte 3H-ouabain binding and digitalis treatment in ethanol addicted patients.

The binding of 3H-ouabain to human erythrocytes was analyzed in a population of hospitalized male ethanol addicted patients under long term digitalis treatment. In the non-alcoholic patient group the long term digitalis treatment induced an increase in Bmax and Kd values; such modification was not observed in the alcoholic patients. Chronic alcohol intake itself induced an increase in 3H-ouabain kinetic parameters. These observations confirm that ouabain binding to human erythrocytes is subject to pharmacological and toxicological regulation and that adaptive changes in peripheral tissues can be useful in predicting possible parallel modifications in other less accessible tissues.

Adult↗
PubMed1987

Concomitant regulation of hippocampal calcium antagonist receptors and calcium uptake by substance P.

The interaction of various neuropeptides with calcium antagonist binding was investigated in rat hippocampus. Among the peptides examined Substance P selectively increased the binding of phenylalkylamine and dihydropyridine calcium antagonists; this action was receptor mediated. No effect was observed with Substance P in other brain areas and with neurotensin and met-enkephalin in all the areas examined. The modification in calcium antagonist binding is functionally paralleled by an area specific increase in voltage-dependent calcium uptake. These data suggest that in hippocampus Substance P may be an endogenous regulator of voltage sensitive calcium channels.

Animals↗
PubMed1987

Acute ethanol effect on calcium antagonist binding in rat brain.

We investigated the effect of acute ethanol administration on voltage-sensitive calcium channels (VSCC) by measuring [3H]nitrendipine ([3H]NTP) binding to crude synaptosomal membrane preparations from different rat brain areas, i.e. cerebral cortex, hippocampus and striatum. Ethanol enhances the number of binding sites shortly after the administration (40 min), then Bmax returns towards control values while the binding affinity increases. Kd decreased peaks 8 h after the oral administration and returns within the range of control values at 36 h. The in vitro addition of ethanol has no effect on [3H]NTP binding at various concentrations up to 600 mM. These results suggest that acute ethanol treatment modifies VSCC supporting the concept that the short-term neurochemical alterations induced by in vivo ethanol administration involve calcium channels.

Animals↗
PubMed1987

Alcohol impairs age-dependent adaptation of human lymphocyte beta-adrenergic receptors.

Lymphocyte beta-adrenergic receptor function and norepinephrine (NE) plasma concentration have been compared in normal subjects and in ethanol-addicted patients of different ages. Direct measurement of the density and properties of beta-adrenoceptors in membrane fractions was performed using the radioligand 125I-Iodocyanopindolol (ICYP). In normal subjects beta-receptor density decreased and norepinephrine plasma concentration increased with age. There was a statistically significant negative correlation between plasma norepinephrine and beta-receptor number. In ethanol-addicted patients the age-related modification in beta-receptor number and the correlation between plasma norepinephrine and beta-receptor density were lost, in spite of the fact that the increase of NE plasma concentration was still present. The ethanol-induced effects in lymphocyte beta-receptor may have consequences on immunological function and may be qualitatively similar to alterations in other tissues not routinely accessible in humans.

Adaptation, Physiological↗
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↗