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C Truzzi

Publications and source records attributed to C Truzzi.

13 recordsLinked to original sources
PubMed2000

Evidence that total extract of Hypericum perforatum affects exploratory behavior and exerts anxiolytic effects in rats.

Clinical trials have extensively reported the ability of Hypericum perforatum extracts to exert a significant antidepressant activity. Hypericin, the main constituent of H. perforatum extract, is no more regarded as the active principle of the antidepressant activity of the drug. Hence, the question of which constituents are involved in the basic activity of the total extract, is still waiting for an answer. In the present study we focused our attention on the potential anxiolytic activity of H. perforatum total extract, and of some pure components such as protohypericin and a fraction containing hypericin and pseudohypericin. Herein we report that the total extract of H. perforatum increases the locomotor activity in the open field and exerts anxiolytic activity in the light-dark test, whereas the single components did not show any effect. Interestingly, the anxiolytic activity of the total extract was blocked by pretreatment of rats with the benzodiazepine antagonist Flumazenil, hence suggesting an implication of benzodiazepine receptor activation in the anxiolytic effect of H. perforatum extract. Electrophysiological studies, performed to gain more information on the mechanism of action, showed that hypericin reduced the GABA-activated chloride currents, while pseudohypericin did an opposite effect. Furthermore, both hypericin and pseudohypericin inhibited the activation of NMDA receptors.

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PubMed1997

Prenatal exposure to methylmercury during late gestation affects cerebral opiatergic system in rat offspring.

Pregnant female rats were orally administered a single dose (8 mg/kg) of methylmercury chloride (MMC) on Day 15 of gestation. The binding characteristics of opioid receptors were studied in the brain of developing rats at different stages of age. An increased density of opioid receptors was found in whole brain of MMC-exposed rats at 21 days (delta receptors) and 60 days (mu and delta receptors) of age, in comparison with matched controls. An enhanced response to morphine administration was detected in MMC-exposed rat offspring at Day 60 of postnatal life, which, however, was not apparently due to an impaired liver metabolization or renal excretion. Hence, it is reasonable to surmise a possible correlation between receptor up-regulation and increased response to pharmacological challenge. These data seem to indicate that neurochemical alterations produced in the rat developing organism by prenatal exposure to methylmercury involve the opiatergic system which undergoes a supersensitivity phenomenon. This effect, which is not detectable in the first postnatal period, shows a delayed onset, being detectable only at the adult stage. These findings seem to indicate that pre- and postnatal methylmercury exposure induces latent neurochemical and behavioral alterations which could last even after the clearance of the metal from the brain.

Animals↗
PubMed1994

Methyl mercury during late gestation affects temporarily the development of cortical muscarinic receptors in rat offspring.

Pregnant Sprague-Dawley rats were treated by gavage with a single dose of 8 mg/kg of methyl mercury on gestational day 15. Offspring of control and treated rats were killed at 14, 21 and 60 days of age. The binding characteristics of muscarinic receptors labelled in cortical membrane preparation by 3H-L-quinuclidinyl benzilate were studied together with the assessment of mercury level in the same brain area. Furthermore, the performance in passive avoidance tasks was evaluated in 8 weeks old rats. Perinatal exposure to methyl mercury significantly reduced the maximum number of muscarinic receptors (Bmax) in the brain of 14 (53%) and 21 day old rats (21%), while this change was no more present in 60 day old rats. This phenomenon seems to be strictly related to the presence of mercury in the cortex since it disappeared with the normalization of mercury levels in the brain. Despite the recovery of muscarinic receptor densities in methyl mercury exposed rats at 8 weeks of age, the avoidance latency was reduced in passive avoidance test as an indication of learning and memory deficits in these animals. Results from this study indicate that prenatal methyl mercury exposure induces latent cognitive dysfunction which does not seem to be related to transient muscarinic receptor alteration found in the early period of postnatal life.

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PubMed1993

Synthesis and antiinflammatory activity of 2,6-bis(1,1-dimethylethyl)phenol derivatives.

The influence of 11 newly synthesized 2,6-bis(1,1-dimethylethyl)phenol derivatives substituted in the 4 position as measured on the carrageenan paw edema assay in Sprague-Dawley rats, was studied using indomethacin as a reference drug. Furthermore we studied the possible interference of few of these compounds on the calcium binding sites by using the specific ligand [3H]-PN 200-110 in "in vitro" experiments. As far as regard the antiinflammatory activity only the compounds 2b, 2j and 2k, dosed at 20 mg/Kg/os, exerted an inhibitory effect on paw edema which was practically equal, after 6 h, to that of indomethacin (approximately 30%) dosed at 2.5 mg/Kg. The compound 2k, however, showed, in comparison with indomethacin and the other new tested compounds, a longer lasting effect, reaching, after 8 h, a 56.7% inhibition of the edema. Finally the above mentioned compounds, when tested alone or in combination with nitrendipine, did not exert any displacing activity on [3H]-PN 200-110 binding to synaptosomal membranes. It is noteworthy however that compound 2e, which incidentally was inactive as antiinflammatory agent, showed a negative allosteric modulatory activity on the ability of nitrendipine to displace [3H]-PN 200-110 binding.

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PubMed1990

Rigid analogs of taurine as potential taurine antagonists.

In this study we tested the potential taurine-antagonistic properties of three rigid analogs of taurine, 3-amino- (1), 3-hydrazino- (2) and 3-aminomethyl-1,2,4-benzothiadiazine-1,1-dioxide (3), which were prepared in our laboratory, using TAG (6-aminomethyl-3-methyl-1,2,4-benzothiadiazine-1,1- dioxide) (4), the only antagonist of taurine so far available, as reference compound in "in vivo" and "in vitro" experiments. Some physicochemical properties of (1), (2) and (3) were studied and the synthesis of TAG (4) was improved with a new preparative method. A dose-effect study performed by injecting intracerebroventricularly (1), (2) and (3) showed that these compounds have none of exciting effects exerted by the high doses of TAG (4). (1) and (3) as well as TAG (4), were found to antagonize the controlateral turning induced by the intracerebro injection of taurine and to potentiate the sedative effect of diazepam. We failed to find specific binding for taurine in different brain synaptic membrane preparations using 3H-taurine as radioligand and taurine, (1) and (3) as binding displacer. (1), (3) and TAG (4) however were found to antagonize the inhibitory effect of taurine on 3H-diazepam binding. These results seem to indicative that at least (1) and (3), which were more extensively studied than (2) because of their better solubility, are taurine antagonists with an apparent better selectivity than TAG (4).

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PubMedDate not supplied

Effect of 2-methyltaurine and its enantiomers on arterial blood pressure.

Taurine has been shown to exert many biological effects. Among them, the ability of this amino acid to induce a reduction of arterial blood pressure, when administered intracerebroventricularly (i.c.v.) to mammals, has been established since a long time ago. To gain further information on the structure-activity requirements for taurine's hypotensive effect, the synthesis of 2-methyltaurine (2-aminopropanesulphonic acid) and the asymmetric synthesis of its enantiomers were performed; the enantiomeric purity of (R)- and (S)-2-methyltaurine was assayed by differential scanning calorimetry (DSC) and HPLC. The findings here reported show that the hypotensive effect elicited by the i.c.v. administration of racemate is mainly due to the (S)-enantiomer. The specificity of this effect was proved by the ability of the taurine antagonist TAG (6-aminomethyl-4H-3-methyl-1,2,4-benzothiadiazine 1,1-dioxide) to prevent it.

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PubMedDate not supplied

Increased brain concentrations of polyamines in rats with encephalopathy due to a galactosamine-induced fulminant hepatic failure.

Polyamine concentrations including putrescine, spermidine and spermine were documented in two brain areas of rats with mild and severe stages of hepatic encephalopathy (HE) due to fulminant hepatic failure induced by galactosamine HC1 injection (3 g kg-1 i.p.). In the mild stage of HE putrescine increased by 3-4 times whereas spermidine and spermine showed a slight increase. The scenario, however, was found to be changed going from the mild to the severe stage of HE, since in this last stage spermidine and spermine showed a further rise while putrescine was found to be significantly lower than in the mild stage of HE in both the brain areas studied. The changes in the ratio among the three polyamines with an enhanced prevalence in the severe stage of HE of spermidine and spermine are likely to be related to the exhaustion of the synthetic pathway of putrescine or to a reduction of the interconversion to this polyamine from spermidine and spermine. Considering that these last two polyamines potentiate the N-methyl-D-aspartate glutamate receptor mediated toxicity and that they might exert neurotoxic effects per se, there are clear reasons for suspecting an implication of the described changes of polyamines in the neurochemical mechanism which sustain HE and to surmise a potential therapeutic effect in this pathology of non-competitive antagonists of polyamine-site on N-methyl-D-aspartate glutamate receptors.

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PubMedDate not supplied

Urine retention due to intra-spinal cord injection of colchicine in rats: improved recovery of bladder function by monosialoganglioside GM1 and nerve growth factor administration.

Intra-spinal cord injection of a low dose of colchicine (2 micrograms/rat) at the lumbar level affects the micturition reflex leading to voiding suppression, bladder hypertrophy and overflow incontinence which lasts about four weeks. The administration of nerve growth factor and monosialoganglioside GM1 normalizes urine output within 3 days and improves recovery of the bladder contraction tested by a cystometric analysis.

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