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Biomedical subjects

F Fadda

Publications and source records attributed to F Fadda.

At least 91 records · Page 5Linked to original sources
PubMed1976

Effect of lithium on dopamine uptake by brain synaptosomes.

Lithium chloride exerts two opposite effects on dopamine uptake by synaptosomes isolated from rat caudate nucleus. Added in vitro, it inhibits dopamine uptake; whereas administered chronically in vivo, it enhances dopamine uptake in vitro. Thus, in vitro, 1, 2.5, 5 and 10 meqiv.l-1 of lithium chloride decrease [3H]dopamine uptake by 13, 17, 25 and 31%, respectively. Synaptosomes isolated from rats treated with lithium chloride for 20 days, show a 23% increase in [3H]dopamine uptake with respect to synaptosomes isolated from control rats. It is suggested that chronic lithium treatment stimulates a compensatory mechanism which overcomes its direct inhibitory effect on [3H]dopamine uptake.

Adrenergic Uptake Inhibitors↗
PubMed1975

Tryptophan-free diet: a new means for rapidly decreasing brain tryptophan content and serotonin synthesis.

Changes in the synthesis rate of brain serotonin are positively correlated with changes in the concentration of brain tryptophan, indicating that the concentration of tryptophan in the whole brain reflects that at sites of serotonin synthesis. In turn, the concentration of brain tryptophan is positively correlated with that of free serum tryptophan (tryptophan is the only amino acid bound to serum proteins) and negatively to that of other amino acids competing with tryptophan for the same transport from blood to brain. Consistently, experiments in rats have shown that treatments which increase free tryptophan in serum (in respect to competing amino acids) also increase brain tryptophan and serotonin turnover. Conversely, the ingestion of diets containing all amino acids except tryptophan cause a dramatic fall in free serum tryptophan and a parallel decline in brain tryptophan and serotonin synthesis. In man the administration of an amino acid mixture lacking trytophan produces a marked depletion in serum tryptophan concentration.

Amino Acids↗
PubMed1973

[Study on the absorption and utilization of D-galactose and D-glucose by liver and muscular tissue in the albino rat].

In order to compare the disposition of D-galactose and D-glucose in various organs of the rat, we have measured the amount of 14C-galactose and 14C-glucose present in the enteric canal, blood, muscle and liver, 2h. after the oral administration of the labelled esoses. Our results show that the two esoses are ebsorbed almost completely and to the same extent by two hours after their administration, Galactose has a longer half-life than glucose, being more slowly utilized in the synthesis of glycogen in liver and muscle.

Animals↗
PubMedDate not supplied

Evidence for a direct action of amphetamine on dopamine metabolism in the rat substantia nigra in vivo.

The intraperitoneal administration of D-amphetamine (0.2--2.5 mg/kg) decreases dihydroxyphenylacetic acid (DOPAC) content not only in the caudate nucleus but also in the substantia nigra. This effect persists both in the substantia nigra and in the caudate nucleus after loss of dopamine-sensitive adenylate cyclase and presumably of dopamine receptors, induced by intrastriatal injection of kainic acid. These results indicate that the effect of amphetamine on DOPAC levels in the nigra is not mediated through a strionigral feedback loop.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Suppression of ethanol intake in ethanol-preferring rats by 1,4-butanediol.

The oral administration of 1,4-butanediol (1,4-BD) at doses ranging from 100 to 300 mg/kg, twice daily, produced a dose-dependent reduction (40 to 85%) in the voluntary ethanol intake in rats selectively bred for high preference for ethanol. Treatment with 1,4-BD did not reduce total fluid intake. Repeated 1,4-BD administration (300 mg/kg twice daily for 7 days) suppressed ethanol intake almost completely. After suspension of 1,4-BD treatment, the inhibitory effect on ethanol intake remained significantly low for 2 days. 1,4-BD failed to inhibit aldehyde dehydrogenase to a concentration of 10 mM in rat liver homogenate.

Alcohol Drinking↗
PubMedDate not supplied

Chronic ethanol consumption induces hypomotility in the portal vein of Sardinian alcohol-preferring rats.

In order to study the physiopathological effects of chronic ethanol intake on the smooth muscle of the vascular system, we have assessed the length-tension relationship in isolated portal veins of Sardinian alcohol-preferring (sP) rats. Significant differences in motor performance were found between sP naive and sP rats exposed to ethanol consumption (12% w/v) for 48 weeks. Isolated portal veins of sP rats which consumed ethanol chronically showed a marked decrease of spontaneous and KCl-induced contraction waves when compared to sP naive rats. At optimum length (140% Lr) for maximal contractile performance, the mean amplitude wave in the portal veins of sP drinker rats was about five times less than in sP naive veins. Furthermore, in the veins of sP drinkers, the active curve showed lower values of tension at each elongation of the vascular segment, the maximum value of active tension (7.32 +/- 0.54 mN) represented a reduction in amplitude of about 32% with respect to sP naive veins. These results indicate that long-term ethanol consumption impairs portal vein motility.

Alcohol Drinking↗
PubMedDate not supplied

Long-term voluntary ethanol consumption induces impairment of the mechanical performance in the papillary muscle of Sardinian alcohol-preferring rats.

The effects of chronic (26 weeks) ethanol consumption on cardiac muscle contractility in Sardinian alcohol-preferring drinkers (sP-D) and Sardinian alcohol-preferring naive (sP-N) rats were investigated. Experiments were carried out 1 week after ethanol administration ceased. Length-tension and force-frequency responses in left ventricular papillary muscles from both sP-D and sP-N rats were recorded in vitro. Papillary muscles were gradually stretched in steps of 5% of the reference (initial) length (L(r)) from 100 to 130% L(r). In sP-D rats, length-tension relationships showed a significant reduction in active tension: at optimal length for maximum active tension (130% L(r)), the developed force value (1.38 +/- 0.36 mN/mg, dry tissue) was 54% lower than that found in sP-N rats (3.16 +/- 0.6 mN/mg, dry tissue). In sP-D papillary muscles, a decrease in contractile behaviour was also observed in force-frequency responses (0.03-120 pulse/min), when compared with sP-N rats; developed force was found to be reduced by about 2.5 times. These results indicate that long-term ethanol consumption impairs the mechanical performance of sP papillary muscle, inducing a negative inotropic effect.

Alcohol Drinking↗
PubMedDate not supplied

Constant absolute ethanol intake by Sardinian alcohol-preferring rats independent of ethanol concentrations.

The present study was designed to evaluate ethanol drinking behaviour in Sardinian alcohol-preferring (sP) and Sardinian alcohol-non-preferring (sNP) rats in the presence of different ethanol concentrations. Ethanol intake was tested under the two-bottle, free-choice regimen and continuous access schedule. Ethanol-naive sP and sNP rats were initially given ethanol solution at the standard, constant concentration of 10% (v/v) for 8 consecutive days (Phase 1). As expected, daily ethanol intake in sP rats rose from 4 to approximately 6 g/kg; in contrast sNP rats consumed < 10 g/kg/day ethanol. Subsequently, an ascending series of ethanol concentrations, ranging from 3 to 60% (v/v), was presented to sP and sNP rats over a 28-day period (Phase 2). At concentrations varying from 7 to 30%, sP rats consumed constant amounts of absolute ethanol per kg of body weight (approximately 6.0 g/kg/day). Daily ethanol intake in sNP rats remained constantly lower than 1.0 g/kg, irrespective of the ethanol concentration. Data from Phase 2 demonstrate the ability of sP rats to precisely adjust daily ethanol intake and support the hypothesis that voluntary ethanol drinking in sP rats is sustained by specific pharmacological effects of ethanol.

Alcohol Drinking↗