PubMed Health⌕ Search

Biomedical subjects

F E Pontieri

Publications and source records attributed to F E Pontieri.

At least 37 records · Page 2Linked to original sources
PubMed1998

Increased motor response to cocaine administration following recovery from chronic corticosterone treatment in the rat.

Several lines of evidence suggest interaction between glucocorticoids and the rat brain dopaminergic system. Here we demonstrate that a two week recovery from chronic high-dose corticosterone treatment potentiates the behavioral response to acute cocaine challenge in the rat. This effect is associated with significant increases of plasma corticosterone levels in response to cocaine. Then, derangement of the hypothalamus-pituitary-adrenal axis, induced by long-term treatment with corticosterone, facilitates the behavioral response to cocaine.

Animals↗
PubMed1997

Dopamine release in striatal slices of rats previously submitted to electroconvulsive shock.

The effects of single and repeated electroconvulsive shock (ECS) on the release of dopamine from rat striatal slices were investigated using the fractional release technique. Experiments were performed 24 h after the single or the last of seven ECS sessions. Repeated, but not single, ECS was associated with reduced dopamine release in response to chemical stimulation. These results suggest that repeated ECS affects the regulation of striatal dopamine presynaptic receptors.

Animals↗
PubMed1997

Increased functional response to cocaine challenge following recovery from chronic corticosterone in the rat.

Several lines of evidence suggest an interaction between glucocorticoids and the rat brain dopaminergic system. Here we demonstrate that a 14-day period of recovery from chronic corticosterone (10 mg/day for 21 consecutive days) potentiates the functional response to acute cocaine challenge in the rat by producing selective metabolic changes in limbic and motor areas, that are not measurable in vehicle-pretreated rats. These data indicate that chronic corticosterone has a long-term facilitatory role in the central effects of cocaine.

Animals↗
PubMed1997

Functional correlates of heroin sensitization in the rat brain.

The aim of the study was to measure the changes in cerebral energy metabolism and c-fos mRNA expression following challenge with heroin in drug-naive rats and in animals previously sensitized to the drug. Acute heroin administration to drug naive-rats produced a generalized metabolic depression. In contrast, challenge with heroin in drug-sensitized rats produced selective metabolic increases in structures belonging to the basal ganglia. These changes were accompanied by increased c-fos mRNA expression in the caudate-putamen nucleus. These results demonstrate that the process of sensitization to heroin is coupled to functional changes that are confined to the subcortical motor circuits of the basal ganglia.

Animals↗
PubMed1997

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↗
PubMed1997

Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common mu1 opioid receptor mechanism.

The effects of the active ingredient of Cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), and of the highly addictive drug heroin on in vivo dopamine transmission in the nucleus accumbens were compared in Sprague-Dawley rats by brain microdialysis. Delta9-THC and heroin increased extracellular dopamine concentrations selectively in the shell of the nucleus accumbens; these effects were mimicked by the synthetic cannabinoid agonist WIN55212-2. SR141716A, an antagonist of central cannabinoid receptors, prevented the effects of Delta9-THC but not those of heroin. Naloxone, a generic opioid antagonist, administered systemically, or naloxonazine, an antagonist of micro1 opioid receptors, infused into the ventral tegmentum, prevented the action of cannabinoids and heroin on dopamine transmission. Thus, Delta9-THC and heroin exert similar effects on mesolimbic dopamine transmission through a common mu1 opioid receptor mechanism located in the ventral mesencephalic tegmentum.

Animals↗
PubMed1997

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↗
PubMed1997

Contribution of blockade of the noradrenaline carrier to the increase of extracellular dopamine in the rat prefrontal cortex by amphetamine and cocaine.

This study was performed to investigate the relative role of noradrenaline (NA) and dopamine (DA) carrier blockade in the effects of psychostimulants on DA transmission in the rat prefrontal cortex (PFCX). To this end, changes of extracellular DA and NA in the PFCX and of extracellular DA in the nucleus accumbens (NAc) were measured following the administration of amphetamine and cocaine, which are known to bind to both DA and NA carriers, or GBR 12909, a selective DA carrier blocker. After non-intravenous injection, amphetamine (0.25 and 0.5 mg/kg, s.c.) and cocaine (5 and 10 mg/kg, i.p.) increased extracellular DA in the PFCX to a larger extent than in the NAc, while the reverse applied to GBR 12909 (2.5 and 5 mg/kg, i.p.). These differences were obtained in spite of the fact that the three drugs elicited at each dose level a similar peak increase of extracellular DA in the NAc. Amphetamine and cocaine also increased extracellular NA in the PFCX and this effect was quantitatively similar to that on extracellular DA in the same area. Intravenous doses of cocaine and GBR 12909, corresponding to those which maintain self-administration in the rat, while equieffective in raising extracellular DA in the NAc, had different effects on extracellular DA in the PFCX. In fact, in contrast to cocaine, GBR 12909 increased extracellular DA in the PFCX to a lesser extent than in the NAc or did not modify it at all. The peak increase of extracellular DA in the PFCX was highly correlated to that of NA in the same area but was poorly correlated to the increase of extracellular DA in the NAc. These results suggest that amphetamine and cocaine increase extracellular DA in the PFCX largely through the blockade of the NA carrier. Direct evidence for this hypothesis was provided by the observation that, when the NA carrier was blocked by reverse dialysis of the PFCX with desipramine (1 microM), cocaine and GBR 12909 lost their differences in the ability to increase extracellular DA in the PFCX.

Animals↗
PubMed1996

Effects of nicotine on the nucleus accumbens and similarity to those of addictive drugs.

The question of whether nicotine, the neuroactive compound of tobacco, is addictive has been open to considerable scientific and public discussion. Although it can serve as a positive reinforcer in several animal species, including man, nicotine is thought to be a weak reinforcer in comparison with addictive drugs such as cocaine and heroin, and has been argued to be habit forming but not addictive. Here we report that intravenous nicotine in the rat, at doses known to maintain self-administration, stimulates local energy metabolism, as measured by 2-deoxyglucose autoradiography, and dopamine transmission, as estimated by brain microdialysis, in the shell of the nucleus accumbens. These neurochemical and metabolic effects are qualitatively similar to those of other drugs, such as cocaine, amphetamine and morphine, which have strong addictive properties. Our results provide functional and neurochemical evidence that there are specific neurobiological commonalities between nicotine and addictive drugs.

Animals↗
PubMed1996

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↗
PubMed1996

Treatment with cyclosporine A promotes axonal regeneration in rats submitted to transverse section of the spinal cord--II--Recovery of function.

Previous reports have suggested a correlation between autoimmunity and abortive axonal regeneration in mammalian CNS. In this study we investigated the effects of immunosuppressive treatment with Cyclosporine A (CyA) (2.5-5 mg/kg/day) on axonal regeneration after complete spinal transection in rats. Partial recovery of function was observed 30 days after surgery in rats treated with CyA, with the presence of incomplete spontaneous locomotion and a positive contact placing reaction. Restoration of somatosensory evoked potentials and positive retrograde fluorescent tracing were also observed. CyA reduced the autoimmune reaction which targeted components of the axons. These results provide further evidence of the role played by autoimmunity in blocking regeneration of fibre tracts in mammalian CNS.

Animals↗
PubMed1995

Intravenous cocaine, morphine, and amphetamine preferentially increase extracellular dopamine in the "shell" as compared with the "core" of the rat nucleus accumbens.

The nucleus accumbens is considered a critical target of the action of drugs of abuse. In this nucleus a "shell" and a "core" have been distinguished on the basis of anatomical and histochemical criteria. The present study investigated the effect in freely moving rats of intravenous cocaine, amphetamine, and morphine on extracellular dopamine concentrations in the nucleus accumbens shell and core by means of microdialysis with vertically implanted concentric probes. Doses selected were in the range of those known to sustain drug self-administration in rats. Morphine, at 0.2 and 0.4 mg/kg, and cocaine, at 0.5 mg/kg, increased extracellular dopamine selectivity in the shell. Higher doses of cocaine (1.0 mg/kg) and the lowest dose of amphetamine tested (0.125 mg/kg) increased extracellular dopamine both in the shell and in the core, but the effect was significantly more pronounced in the shell compared with the core. Only the highest dose of amphetamine (0.250 mg/kg) increased extracellular dopamine in the shell and in the core to a similar extent. The present results provide in vivo neurochemical evidence for a functional compartmentation within the nucleus accumbens and for a preferential effect of psychostimulants and morphine in the shell of the nucleus accumbens at doses known to sustain intravenous drug self-administration.

Amphetamine↗
PubMed1995

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↗
PubMed1995

Selective metabolic activation by apomorphine in striosomes of denervated striatum in MPTP-induced hemiparkinsonian monkeys.

Results of previous studies have suggested differences in the regulatory mechanisms in striatal striosomes and matrix following interruption of dopaminergic input to the striatum by MPTP in the monkey. In the present study we have investigated the possibility that stimulation of dopamine receptors by apomorphine modifies glucose metabolism differentially in the two striatal compartments of unilaterally MPTP-lesioned monkeys. Apomorphine treatment was found to result in higher rates of glucose utilization in the denervated striatum than in the intact hemisphere. Furthermore, the effect was more robust in the striosomes than in the matrix, thus providing evidence for differential functional and/or metabolic regulation in striatal striosomes and matrix in parkinsonian syndromes.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1994

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↗
PubMed1993

Local cerebral glucose utilization after D1 receptor stimulation in 6-OHDA lesioned rats: effect of sensitization (priming) with a dopaminergic agonist.

In rats bearing unilateral 6-hydroxydopamine (6-OHDA) lesions of the dopaminergic nigro-striatal neurons, a single administration of a D-2 agonist (LY 17155) potentiates the contralateral turning induced by a D-1 agonist (SKF 38393). To identify the neural substrate of this form of sensitization (priming), we studied the local cerebral glucose utilization (lCMRglc) in 6-OHDA lesioned animals treated, 3 days apart, as follows: (1) saline-saline, (2) LY 171555-saline, (3) saline-SKF 38393 and (4) LY 171555-SKF 38393. The unilateral 6-OHDA lesion per se (Sal-Sal) produced increases in lCMRglc in the globus pallidus (GP) and in the lateral habenula (LH) of the lesioned hemisphere. lCMRglc in LY-Sal group were similar to those measured in the Sal-Sal group. Administration of SKF 38393 to drug-naïve rats (Sal-SKF) abolished the lesion-induced metabolic asymmetry in the LH but did not have any effect on the GP; furthermore, it increased lCMRglc in the substantia nigra pars reticulata (SNr) of the lesioned side. After priming with LY 171555, administration of SKF 38393 (LY-SKF) produced marked metabolic asymmetries by increasing lCMRglc in the SNr and entopeduncular nucleus (EP), and decreasing it in the LH of the lesioned side. These changes were also significant when compared to the corresponding values of the other experimental groups. Again, in LY-SKF group no modification of the lesion-induced metabolic asymmetry in the GP was found.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Metabolic mapping of the pharmacological and toxicological effects of dopaminergic drugs in experimental animals.

Functional consequences of pharmacological and toxicological manipulations of the dopaminergic systems were evaluated by means of the 2-[14C]deoxyglucose (DG) method for measuring local rates of cerebral glucose utilization. Administration of dopamine agonist drugs modifies glucose metabolism in selected brain areas. Several factors, such as the compound used, the dose, length, and modality of the treatment, and the interval of time between the end of the treatment and the measurement of glucose utilization, contribute to define the topography and intensity of the changes. The differences refer to distinct activation of subtypes of dopamine receptors, to secondary involvement of other neurotransmitter receptor systems, and to modification of the receptor sensitivity occurring during the treatment. Other variables that interfere with the motivated behavior induced by psychostimulants may also affect the metabolic pattern. A few changes in glucose utilization are, however, common to most dopamine agonist drugs. High doses, which induce stereotypic behavior, produce metabolic changes in the extrapyramidal system. Low doses of psychostimulants, which elicit locomotion and exploratory behavior and produce reinforcement, increase glucose metabolism in the limbic system, particularly in the nucleus accumbens. Metabolic mapping in monkeys bearing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced lesions of the dopaminergic areas in the brainstem contributed to define the key role of the striatopallidal pathway in the production and maintenance of the motor abnormalities that characterize parkinsonism. Metabolic patterns associated with unilateral 6-hydroxydopamine lesion of the nigrostriatal neurons in the rat are modified by dopamine agonist drugs. Specific changes are produced by selective D1 or D2 agonists. In rats bearing unilateral 6-hydroxydopamine lesion, the DG method also revealed functional effects produced by the interaction between D1 and N-methyl-D-aspartate receptors.

Animals↗