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E Mosca

Publications and source records attributed to E Mosca.

17 recordsLinked to original sources
PubMed1992

Presynaptic dopamine autoreceptors and second messengers controlling tyrosine hydroxylase activity in rat brain.

In brain areas enriched of dopaminergic nerve terminals presynaptic dopamine (DA) autoreceptors control the state of activation of tyrosine hydroxylase (TH) by regulating the extent of phosphorylation of the enzyme. Evidence is presented indicating that this autoinhibitory control may involve a decrease in the cyclic AMP-dependent activation of TH through an inhibitory coupling of presynaptic DA autoreceptors to adenylate cyclase. As indicated by the insensitivity of the DA inhibition of TH to changes in the extracellular concentrations of Ca++, to the addition of the Ca++ ionophore A 23187 and of different K+ channel blockers, a reduction of Ca++ influx and an increase in the K+ channel activity do not seem to be involved in the presynaptic regulation of TH activity by DA autoreceptors at least under basal conditions.

Animals↗
PubMed1990

Alcohol-preferring rats: genetic sensitivity to alcohol-induced stimulation of dopamine metabolism.

The effect of ethanol on brain dopamine (DA) metabolism in the caudate nucleus (CN), olfactory tubercle (OT) and medial prefrontal cortex (MPFC) was compared in two selectively bred rat lines, one ethanol preferring and the other ethanol nonpreferring. Male rats from the 16th and 17th generations of both lines that never experienced ethanol beforehand were used. No differences in the basal concentrations of DA and its metabolites, DOPAC and HVA, in the above brain regions were found between the two lines. The oral administration of 2 g/kg of ethanol to ethanolnonpreferring rats increased DOPAC and HVA and reduced DA levels in the CN and OT but was ineffective in the MPFC. On the other hand, ethanol administration to ethanol-preferring rats decreased DA content and increased DOPAC and HVA levels, not only in the CN and OT, but also in the MPFC. Moreover, the changes induced by ethanol on DA metabolism in the latter group were significantly greater than in ethanol nonpreferring rats. These results indicate that ethanol preferring rats have a genetic high sensitivity to the ethanol effect on DA metabolism, and suggest that such a trait might play a role in ethanol preference.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Voluntary alcohol drinking increases brain dopamine metabolism in rats.

The effect of ethanol on dopamine (DA) metabolism in two selectively bred lines of rats, one alcohol-preferring (sP) and the other--non-preferring (sNP), was studied. Ethanol administration (2 g/kg per os) produced in the two lines of rats a decrease of DA content and an increased concentration of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the caudate nucleus, olfactory tubercle and medial prefrontal cortex in both lines, but the effect was significantly greater in sP than in sNP rats. Moreover, in sP rats, the voluntary consumption of ethanol increased DOPAC and HVA levels in the above areas. In these animals, DOPAC and HVA accumulation was associated with a small depletion in DA content, suggesting that ethanol releases DA from stores.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Different effects of the calcium antagonists nimodipine and flunarizine on dopamine metabolism in the rat brain.

The effect of two calcium antagonists, nimodipine and flunarizine, on striatal dopamine (DA) metabolism in rats was compared. Flunarizine (5-20 mg/kg i.p.) caused a dose-dependent increase in the DA metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC) in the caudate nucleus. Following the 20 mg/kg dose, DOPAC levels were maximally elevated by about 50% from 2 to 12 hrs after treatment. On the contrary, nimodipine at the dose of 20 mg/kg i.p. produced a modest decrease in DOPAC levels. Neither calcium antagonist modified DA content. However, both nimodipine and flunarizine, at the dose of 20 mg/kg, markedly reduced the accumulation of DOPAC in the caudate nucleus induced by haloperidol (1 mg/kg). It is suggested that flunarizine, but not nimodipine, has a neuroleptic-like action, whereas the two calcium antagonists have in common the ability to attenuate the hyperactivity of DA neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Effect of spontaneous ingestion of ethanol on brain dopamine metabolism.

The effect of ethanol, either administered by gavage or voluntarily ingested, on brain dopamine (DA) metabolism was studied in alcohol-preferring and alcohol non-preferring rats. In alcohol non-preferring rats ethanol administration (2 g/kg) increased 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) and reduced DA levels in the caudate nucleus and olfactory tubercle but was ineffective in the medial prefrontal cortex. In alcohol-preferring rats ethanol effect was greater than in non-preferring animals and ethanol influenced DA metabolism also in the medial prefrontal cortex. The effect of voluntary ethanol ingestion was studied in alcohol-preferring rats trained to consume their daily fluid intake within 2 hrs. Voluntary ingestion of ethanol (3.1 +/- 0.7 g/kg in 1 hr) increased DA metabolites and reduced DA levels in the caudate nucleus, olfactory tubercle and medial prefrontal cortex. The results suggest that voluntary ethanol ingestion increases the release of DA from nigro-striatal and meso-limbic DA neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Suppression by gamma-hydroxybutyric acid of ethanol withdrawal syndrome in rats.

The ability of gamma-hydroxybutyric acid to suppress ethanol withdrawal syndrome was tested in male rats rendered physically dependent on ethanol by several intragastric administrations of ethanol (9-15 g/kg daily for 7 days). Gamma-hydroxybutyrate (0.25, 0.50 and 1.00 g/kg i.p.), administered 8 hr after the last ethanol dose, produced a dose-dependent inhibition of withdrawal signs such as tremors and audiogenically-induced seizures; the highest dose tested suppressed all ethanol withdrawal symptoms.

Animals↗
PubMed1987

Ethanol prevents stress-induced increase in cortical DOPAC: reversal by RO 15-4513.

Electric foot-shock increased DOPAC and decreased DA levels by about 70 and 20% respectively in the medial prefrontal cortex in rats. Pretreatment with diazepam (5 mg/kg IP) or ethanol (1.2 g/kg orally) prevented these stress-induced changes. The protective effect of diazepam and ethanol was eliminated by RO 15-4513 (5 mg/kg IP) a partial inverse benzodiazepine agonist.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Inhibition of voluntary ethanol intake in rats by a combination of dihydroergotoxine and thioridazine.

Dihydroergotoxine (DHET) decreased voluntary ethanol intake in rats selected for their stable ethanol preference (mean daily ethanol intake 8 g/kg). DHET inhibition was markedly potentiated by thioridazine. The potentiation is explained with a synergistic inhibitory effect on dopaminergic transmission: that is, DHET acting on dopamine (DA) autoreceptors and thioridazine preferentially inhibiting postsynaptic DA receptors.

Alcohol Drinking↗
PubMed1985

Suppression by progabide of ethanol withdrawal syndrome in rats.

Progabide, a specific and clinically used GABA receptor agonist, was tested for its ability to suppress ethanol withdrawal syndrome. Male rats were rendered physically dependent on ethanol by feeding for 12 days on a liquid diet in which ethanol isocalorically replaced dextrose. Progabide (100-400 mg/kg i.p.), administered 8 h after ethanol was withdrawn, produced a dose-related inhibition of both tremors and audiogenically induced seizures. A single dose of 400 mg/kg of progabide completely suppressed all ethanol withdrawal reactions. Seizures were more sensitive to the drug than tremors. The results support the view that a decrease in GABA transmission plays a role in ethanol withdrawal symptoms and suggest that progabide may be tested as a possible treatment of ethanol withdrawal syndrome in man.

Acoustic Stimulation↗
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

Ethanol-stress interaction on dopamine metabolism in the medial prefrontal cortex.

The effect of foot-shock and ethanol (2 g/kg per os) and the combination of the two on dopamine (DA) metabolism in the medial prefrontal cortex (MPFC) was studied in rats. Electric foot-shock stress (20 min stimulation) decreased DA concentration by 30% and increased dihydroxyphenylacetic acid (DOPAC) concentration by 65%. Ethanol (2 g/kg orally) decreased DA concentration by 20%, but, unlike foot-shock, failed to modify DOPAC levels. Neither treatments modified homovanillic acid (HVA) levels. The combination of ethanol (30 min before shock) and foot-shock produced about a 50% depletion of DA content and 30% increase in HVA, but no change in DOPAC levels. It is suggested that both ethanol and foot-shock activate DA release in the MPFC, but ethanol decreases DA retrieval by nerve terminals and, therefore, prevents intraneuronal deamination of the amine.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

[Non-endocarditic mitral insufficiency].

A case of non endocarditic mitral insufficiency in a 76 years old woman is described. After an extensive pathogenetical introduction, a comparison is made between clinical features of this case an its pathogenetical possibilities. The conclusion is drawn that there are most probabilities for an atherosclerosis of the antero-medial limbus of the mitral valve, arising from a coexisting atherosclerotic mild stenosis of the aortic valves.

Aged↗
PubMedDate not supplied

[Motor rehabilitation in the aged. Clinical evaluation of the physiokinesis therapy department at a geriatric division for acute diseases].

Physiokinesitherapeutic results obtained in a geriatrics division showed that aged subjects with motor is injuries have the same chance of recovery as those in middle age. The time required for each stage and the overall duration of treatment are more or less the same. No special technological differences are involved, though close psychological training is necessary, and encouragement of the open brain-environment system may useful. Restrictions, though hardly even contraindications, may be encountered in the form of other infirmities more commonly associated with age. It is clear, therefore, that physiotherapy should always be attempted in the aged, in keeping with the clinical picture as well as the motor lesions involved. Physiokinesitherapy Geriatrics.

Age Factors↗
PubMedDate not supplied

[Clinico-radiological considerations on senile atrophic gastritis].

59 cases of patients in geriatric age have been examined in which clinical symptomatology, radiographic exams and laboratory data had indicated the possible presence of gastric neoplasia. The repetition of the radiographic exam after giving methoclopramide for some days has demonstrated, excluding neoplastic lesion, that it was senile atrophic pseudo-tumoral gastritis. The diagnosis has been confirmed in numerous cases by gastroscopy with biopsy.

Age Factors↗
PubMedDate not supplied

[Current knowledge on memory in the elderly].

In geriatric practice, much thought must be given to initial changes in intelligence and memory due to old age and often suddenly aggravated by dysmetabolic and circulatory disease. Awareness of the memory faculty in the elderly is vital in clinical practice for the purposes of pharmacological and psychological designed to reduce the intellectual decline of the patients. This deficiency in mental personality is an important limitation to rehabilitation which remains the aim of medical attention.

Age Factors↗