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F Passarelli

Publications and source records attributed to F Passarelli.

At least 37 records · Page 2Linked to original sources

Differential effects of acute administration of clozapine or haloperidol on local cerebral glucose utilization in the rat.

We employed the [14C]2-deoxyglucose method in order to map local brain metabolic activity of rats administered 1, 5, or 20 mg/kg of clozapine, or 0.5 mg/kg of haloperidol, as compared to saline. Clozapine produced a dose-dependent reduction of glucose utilization. At the dose of 1 mg/kg, the effects were limited to limbic areas. An additional number of structures were significantly affected following administration of 5 mg/kg (the whole hippocampal formation and septal area, and cortical limbic areas). The dose of 20 mg/kg markedly reduced glucose utilization in most of the areas examined. Haloperidol (0.5 mg/kg) reduced glucose utilization of the orbital cortex, hippocampal formation and septal area, globus pallidus, amygdala, ventral thalamus, and substantia nigra reticulata. The results show that acute administration of clozapine or haloperidol are associated with different distribution patterns of altered cerebral energy metabolism. Clozapine differently from haloperidol, reduces energy metabolism of the nucleus accumbens and other limbic areas. Haloperidol, but not clozapine (1 or 5 mg/kg), affects the substantia nigra reticulata.

Animals↗

Electroconvulsive shock blocks the opioid-mediated inhibition of dopamine release in rat striatal slices.

The fractional release technique was applied to investigate the effects of single electroshock (ECS) on the opioid-mediated inhibition of dopamine release in rat striatal slices. Animals were submitted to ECS 24h before the experiments. The results demonstrate that pre-treatment with ECS suppresses the inhibition of dopamine release mediated by kappa opioid receptors. These data suggest that single ECS treatment modifies the sensitivity of the kappa opioid receptors located on the presynatic dopamine terminals in the rat striatum.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

[Histopathologic changes of cancer of the rectum after neoadjuvant radio-chemotherapy. Anatomo-radiologic correlation and prognostic implications].

The histopathologic study of 24 specimens of radiated rectal cancers suggested new histologic criteria to define tumor regression after neo-adjuvant therapy. Better than traditional UICC staging system (pTNM), such criteria have identified those patients at higher risk of failure. Moreover, the study has confirmed the known difficulties of imaging studies in assuring an accurate staging of radiated rectal cancer before surgery.

Adult↗

Differential expression of heat shock protein (HSP70) mRNAs in rat cells.

Heat shock treatment in PC12 cells induces the synthesis of two HSP70 transcripts of 2.55 and 3.05 kb in size, while only a 70-kDa protein is shown by SDS-PAGE. Using reverse transcription-polymerase chain reaction strategy, two mRNA species were amplified from heat-shocked PC12 cells and sequenced. Both cDNAs revealed the same open reading frame encoding a single predicted 641-amino-acid polypeptide of about 70 kDa. The two 3' untranslated regions of the two mRNAs were completely different in both length and composition. Expression of the mRNA of the two corresponding genes and that of another rat HSP70 family member was investigated in PC12, Rat1 cells, and lung fibroblasts. Northern blot analysis revealed that the 2.55- and the 3.05-kb related gene transcripts are differentially expressed in the rat cell lines tested, while the third member of the subfamily is not induced. The single-copy nature of the three genes is also confirmed by Southern blot analysis.

Animals↗

Intravenous morphine increases glucose utilization in the shell of the rat nucleus accumbens.

The [14C]2-deoxyglucose method was applied to measure the effects of the acute intravenous administration of morphine sulphate (0.2-0.4 mg/kg) on cerebral glucose utilization in rats. Morphine produced dose-dependent increases of glucose metabolism in the shell of the nucleus accumbens, without affecting functional activity in any other brain area. These results provide further evidence for the preferential effects of intravenously abused substances in the shell of the nucleus accumbens.

Animals↗

Functional correlates of repeated administration of cocaine and apomorphine in the rat.

The [14C]2-deoxyglucose method was applied to measure the effects of repeated (8 consecutive days) administration of apomorphine (0.5 mg/kg/day s.c.) or cocaine (15 mg/kg/day i.p.) on cerebral glucose utilization in freely moving rats. Altered rates of glucose utilization were measured in extrapyramidal motor areas, such as the globus pallidus, entopeduncular nucleus, subthalamic nucleus, substantia nigra and lateral habenula of both cocaine- and apomorphine-treated rats. Furthermore, cocaine-treated animals displayed increased glucose metabolism in the mesolimbic dopaminergic projections, such as nucleus accumbens and olfactory tubercle, and in the hippocampus. These results suggest that altered functional activity within the dopaminergic mesolimbic system may play a role in the process of sensitization to psychomotor stimulant drugs.

Animals↗

Psychostimulant drugs increase glucose utilization in the shell of the rat nucleus accumbens.

The nucleus accumbens (NAc) is a heterogeneous area, divided into a 'shell' and a 'core' on the basis of morphological and histochemical criteria. Moreover, the two portions have different anatomical connections. In order to test whether the two portions of NAc are functionally distinct, we measured local cerebral glucose utilization in rats administered intravenously with cocaine (1 mg kg-1) or amphetamine (0.5 mg kg-1). The results of the study show that, at these dosages, both drugs increase glucose utilization in the shell, but not in the core of NAc. This differential effect might reflect functional differences between the two portions of NAc, probably relevant to the abuse liability of psychostimulants.

Amphetamine↗

Effects of electroconvulsive shock on the levels of hsp70 and hsc73 mRNA in the rat brain.

We evaluated the effects of electroconvulsive shock (ECS) on the expression of two genes encoding 70 kDa stress proteins, in the rat brain. The study was carried out by in situ hybridization using oligonucleotide probes specific for either the constitutively expressed hsc73, or the strictly inducible hsp70 gene. Rats were submitted to single or repeated (7 days, one session for each day) sessions of Electroconvulsive Shock. Animals were sacrificed at various time after treatment. ECS enhanced the basal expression of hsc73 in limbic areas, such as dentate gyrus, CA3, and median habenular nucleus. ECS induced hsp70 mRNA, which was not detectable in control animals, specifically in the Dentate Gyrus. The effect was present 2 h following treatment. Both single and repeated ECS were similarly effective. The finding likely reflects neuroadaptive local changes associated with a generalized seizure activity.

Animals↗

Somatostatin mRNA in the hippocampal formation following electroconvulsive shock in the rat.

The effect of electroshock on the brain levels of somatostatin mRNA were evaluated by in situ hybridization using a selective oligonucleotide probe. Rats were submitted to single or repeated (7 days, one session for each day) sessions of electroshock. There was a marked increase of the expression of somatostatin mRNA in the hippocampal formation, mostly in the multiform layer of the hilus of the dentate gyrus, following repeated but not single electroshock. Our findings show that repeated ECS is associated with increase in the synthesis of somatostatin. The results also support previous data indicating that the hippocampal formation is selectively affected by the treatment.

Animals↗

Parkinson's disease and somatosensory evoked potentials: apomorphine-induced transient potentiation of frontal components.

We recorded somatosensory evoked potentials (SEPs) to median nerve stimulation from parietal and frontal districts in 32 patients with Parkinson's disease by evaluating latency/amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and 10, 20, 30, and 60 minutes after subcutaneous administration of apomorphine chloride. The frontal complex N30-P40 was smaller than normal in 17 patients in baseline recordings. Following apomorphine, the parietal responses did not significantly vary in amplitude, but the frontal complex showed a remarkable amplitude potentiation in 22 of 32 patients (68.7%, p < 0.001), 19 of whom were also improving clinically. Amplitude potentiation was evident 10 minutes after apomorphine and faded away nearly in parallel with the end of its clinical efficacy. There were no SEP changes in three healthy controls after apomorphine.

Adult↗

Effect of electroconvulsive shock treatment on the opioid-mediated inhibition of serotonin release in rat hippocampal slices.

We investigated the influence of electroconvulsive shock treatment on the opioid-mediated inhibition of serotonin (5-HT) release. The overflow of [3H]serotonin elicited by high potassium (30 mM) in superfused slices of rat hippocampus was significantly inhibited in the presence of two agonists, mu-selective [D-Ala2,N-methyl-Phe4,Gly5ol]enkephalin (DAGO) and delta-selective [D-Pen2,D-Pen5]enkephalin (DPDPE) in control animals. The repeated (once daily for 7 days) electroconvulsive shock treatment significantly reversed the inhibitory effect of both DAGO and DPDPE. Single electroconvulsive shock (1 day) had no effect on DAGO inhibition, on the contrary a trend to antagonism of the DPDPE effect was reported. These results suggested that the opioids are associated with the experimental induced seizures and that the ECS treatment might regulate the serotonin release throughout the opioid receptor system.

Analgesics↗

Propofol and thiopentone for caesarean section revisited: maternal effects and neonatal outcome.

In 56 women undergoing elective caesarean section, general anaesthesia was induced with either propofol 1% or thiopentone 2.5% followed by 50% nitrous oxide in oxygen and isoflurane 0.75% until delivery. In the thiopentone group the arterial pressure rose following tracheal intubation and skin incision, while in the propofol group there was a significant tendency to hypotension immediately following induction of anaesthesia. There were differences in electroencephalogram (EEG) between the groups, while laryngoscopy, intubation and surgical stimulation had no effect on EEG pattern. Recovery after anaesthesia did not differ between groups. None of the patients had recall of the intraoperative period, but 53% of patients induced with propofol showed signs of light anaesthesia between induction and delivery. Neonates in the propofol group had lower Apgar scores 1 min after birth than those in the thiopentone group, but these differences were no longer significant at 5 min. No differences were noted in neurobehavioural status at 1, 4 and 24 h.

Journal Article↗

Repeated electroconvulsive shock increases glial fibrillary acidic protein, ornithine decarboxylase, somatostatin and cholecystokinin immunoreactivities in the hippocampal formation of the rat.

Rats were submitted to single or repeated (7 days, one session for each day) sessions of electroconvulsive shock. A computer-assisted morphometric and microdensitometric analysis of glial fibrillary acidic protein-, ornithine decarboxylase-, somatostatin- and cholecystokinin-like immunoreactivities was performed in the hippocampal formation and other brain areas. The results of the study showed a significant increase of the intensity of the immunostaining for glial fibrillary acidic protein, ornithine decarboxylase, somatostatin and cholecystokinin in the hippocampal formation and distinctively in the dentate gyrus following repeated, but not single, electroconvulsive shock. No significant change was found in the number of somatostatin- and cholecystokinin-like immunoreactive cell bodies in any hippocampal subregion and in the number of glial cells in the hilus of dentate gyrus in rats treated with single or repeated electroconvulsive shock. It is a distinct possibility that the observed increase in the content of the neuropeptides in the hippocampal formation reflects a compensatory response of the brain to seizure-inducing stimuli and that such an increase may play a role in the therapeutic effect of electroconvulsive shock.

Animals↗

CT indications for surgery and evaluation of prognosis in patients with spontaneous intracerebral haematomas.

This study retrospectively analyzes the CT findings of 50 patients with spontaneous intracerebral haematomas and correlates them with the clinical condition at admission and the outcome. The volume of the haematoma was well correlated with the outcome and was a very useful indicator for surgery. In patients with haematoma volume lower than 25 ml and above 80 ml there was no indication for surgery; in patients with haematoma volume between 25 and 50 ml the operation does not significantly modify the survival rate, but favours a more rapid and complete recovery of the neurological deficits, whereas a haematoma volume between 50 and 80 ml favours the rate of survival.

Adult↗

A two-step mechanism by which corticotropin-releasing hormone releases hypothalamic beta-endorphin: the role of vasopressin and G-proteins.

It is well established that in the pituitary gland corticotropin-releasing hormone (CRH) stimulates the release of beta-endorphin (beta-E) via a cAMP-linked mechanism. Studies of the mechanisms underlying the CRH stimulation of beta-E release from rat hypothalamic slices perifused in vitro are reported in this paper. The data indicate that both a cAMP-dependent and non-cAMP-dependent mechanism mediate the action of CRH in the hypothalamus. The presence of a cAMP-linked mechanism was suggested by the finding that cholera toxin (0.1-10 nM) and forskolin (2.5 x 10(-6) M), both of which act to raise intracellular cAMP levels, stimulated the release of beta-E. In both cases, no further stimulation was seen upon addition of CRH (10(-8)M). However, it was also found that preincubation of the tissue with pertussis toxin (PTX; 100 ng/ml) prevented both the CRH- and forskolin-stimulated release of beta-E. This indicated that, in addition to the cAMP-linked mechanism, a further messenger system which is connected to a PTX-sensitive G-protein may also play a role. The latter observation also implied that a further substance, which utilizes a separate second messenger system, might be involved in the CRH stimulation of beta-E release. In this regard the role of arginine vasopressin (AVP) was investigated due to the known interaction between CRH and AVP in the pituitary gland. AVP (10(-12) to 10(-6)M) itself potently and dose-dependently stimulated beta-E release, producing a maximal increase of 220% above basal levels. The AVP-induced release of beta-E was abolished in PTX-pretreated hypothalami. The apparently obligatory requirement of AVP for the CRH-stimulation of beta-E release was illustrated by the finding that blockade of AVP receptors using the AVP antagonist d(CH2)5 [Tyr(OEt)2,Val4]-AVP almost completely attenuated the CRH-stimulated release of beta-E. Furthermore, in the presence of a high concentration of AVP (10(-6)M) no further stimulation of release was seen with CRH (10(-8)M). These data therefore strongly indicate that CRH acts via the intermediacy of AVP to release beta-E from hypothalamic slices in vitro and that two separate second messenger systems are involved: a cAMP-linked mechanism connected to a cholera toxin-sensitive G-protein (CRH) and a second system linked to a PTX-sensitive G-protein (AVP).

Animals↗

Mu and delta opioid receptors inhibit serotonin release in rat hippocampus.

We studied the influence of opioid agonists on the release of serotonin (5-HT) elicited by K+ (20 mM) in superfused slices of rat hippocampus. K+-evoked outflow of serotonin was inhibited significantly up to 50% in the presence of the mu-selective agonist [D-Ala2,N-methyl-Phe4,Gly5-ol]enkephalin (DAGO) and of the delta-selective agonist [D-Pen2,D-Pen5]enkephalin (DPDPE). U50,488H a selective kappa agonist, at concentrations between 0.1 to 1 microM, produced an inhibition of 5-HT-release lower than that observed in the presence of mu and delta agonists. The delta antagonist ICI 174,864 (N,N-diallyl-Tyr1,Aib2,Aib3)Leu-enkephalin potently inhibited the effect of DPDPE but did not affect the inhibition produced by DAGO. In contrast, the mu-selective antagonist D-Phe-Cys-Tyr-D-Trp-Nle-Thr-Pen-Thr-NH2 at 1 microM significantly reversed the inhibitory effect produced by a maximal dose of DAGO (0.1 microM) but not the corresponding effect produced by a maximal dose of DPDPE (1 microM). Naloxone was a competitive antagonist of DAGO but noncompetitive antagonist of DPDPE. Treatment of hippocampal slices with pertussis toxin did not alter the K+-evoked release of 5-HT but abolished the inhibitory effect of both DAGO and DPDPE.

Animals↗

Pertussis toxin inactivates the presynaptic serotonin autoreceptor in the hippocampus.

The serotonin (5-HT) agonists, D-lysergic acid diethylamide (LSD) and 5-methoxytryptamine (5-Me-O-T), dose dependently inhibited the K+-evoked outflow of [3H]5-HT from preloaded rat hippocampal slices in vitro, indicating activation of the 5-HT autoreceptor. However, this effect was abolished in slices pretreated with pertussis toxin. It is thus concluded that the 5-HT autoreceptor in the hippocampus is coupled to G proteins.

5-Methoxytryptamine↗