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A Groppetti

Publications and source records attributed to A Groppetti.

At least 37 records · Page 2Linked to original sources
PubMed1983

Presence of opiate receptors on striatal serotoninergic nerve terminals.

After degeneration of serotoninergic neurons induced by either transection of the ascending neuronal pathways originating from the nucleus raphe dorsalis or intraventricular 5,6-dihydroxytryptamine administration, the number of binding sites for [3H]D-Ala2, Met5-enkephalinamide was significantly reduced. This decrease in binding sites does not seem to be related to the opiate receptors present on dopaminergic terminals, nor is it due to a simple decrease in serotoninergic neuronal tone, since after p-chlorophenylalanine (100 mg/kg X 4 days) the number of striatal binding sites for the opiate ligand was not diminished. On the other hand, shortly after mechanical interruption of the raphe-striatal serotoninergic fibers, at a time when the metabolic processes are still functioning in the lesioned neurons, morphine still increased the striatal content of 5-hydroxyindoleacetic acid. These results suggest the presence of opiate receptors on striatal serotoninergic terminals, where they may modulate the presynaptic activity of these neurons.

Animals↗
PubMed1983

Opiate tolerance and dependence is associated with a decreased activity of GTPase in rat striatal membranes.

In vitro addition of opiates to rat striatal membranes significantly stimulated a low Km GTPase activity. The opioid peptide (D-Ala2, Met5) enkephalinamide was ten folds more active than morphine to elicit the effect while the kappa agonist ethylketocyclazocine was almost inactive. Opiate stimulation was antagonized by naloxone, indicating that specific opiate receptors were involved. Moreover, the effect was stereospecific since levorphanol significantly increased the GTPase activity while its enantiomer dextrorphan was completely inactive, even at concentrations as high as 100 microM. On the other hand, opiates have been reported to inhibit striatal adenylate cyclase whose activity is dependent on GTP. Our data suggest therefore that stimulation of GTPase can be the mechanism by which opiates lower adenylate cyclase activity. This view is supported by the finding that in striatal membranes of rats made tolerant-dependent to morphine, GTPase activity was significantly decreased. Narcotic tolerance and dependence is in fact associated to hyperactivity of adenylate cyclase. It is concluded that GTPase could be the primary site on which opiates act to produce the acute or chronic effects on adenylate cyclase activity.

Animals↗
PubMed1982

Interactions between serotonergic and enkephalinergic neurons in rat striatum and hypothalamus.

We report evidence for an interaction between serotonergic and enkephalinergic neurons in rat striatum and hypothalamus. The administration of drugs such as p-chlorophenylalanine (PCPA), 5,6-dihydroxytryptamine (5,6-DHT) and fenfluramine that lower the striatal and hypothalamic serotonin (5-HT) content caused an increase in Met-enkephalin-like immunoreactive material (ME-IR) in these brain areas. Moreover, chronic treatment with PCPA induced an increase in the number of striatal [3H][D]Ala2,Met5]enkephalinamide binding sites. These observations suggest that serotonergic neurons modulate the functional activity of enkephalinergic neurons in the rat striatum and hypothalamus. The significance of this interaction is discussed.

Animals↗
PubMed1979

Relevance of GABA in the nigrostriatal system.

In conclusion, even though the mutual integration of intrastriatal circuits remains an open question, the electrophysiological and neurochemical approaches seem to provide valid support toward understanding the complexity of these systems. Recent findings seem to indicate that, besides a dopaminergic and cholinergic link, interactions between DA and GABA neurons may be operative within the striatum. An understanding of these functional interplays may facilitate future attempts aimed at clarifying the electrophysiological discrepancies concerning the inhibitory or excitatory action of DA on the target cells in this brain structure. Studies on the functional roles of pathways projecting from striatum to substantia nigra have indicated that these may be implicated in the regulation of nigral efferents to other brain nuclei and that they do control striatal DA activity through feedback mechanisms.

Animals↗
PubMed1978

Significance of dopamine metabolites in the evaluation of drugs acting on dopaminergic neurons.

The effect of various drugs was studied on 3-methoxytyramine (3-MT) concentrations in rat striatum. The drugs were chosen for their ability to interfere with the dopaminergic system at different levels. Dopamine (DA) acidic metabolites, i.e. homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), were also measured. Changes of 3-MT, unlike those of DOPAC and HVA, seem to reflect the functional activity of dopaminergic neurons. In fact drugs believed to increase or decrease DA content in the synaptic cleft produce predictable changes of striatal 3-MT. Thus cocaine, nomifensine and d-amphetamine increase 3-MT concentrations while gamma-butyrolactone, alpha-methyltyrosine and apomorphine decrease it.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Behavioural effects of a new non-phenylethylamine anorexigenic agent: mazindol.

Mazindol, a new anorexigenic agent which possesses a different chemical structure from phenylethylamine derivatives such as amphetamine, causes anorexia along with increases in locomotor activity and body temperature. Mazindol also induces stereotyped behaviour and, if injected into rats with unilateral nigro-striatal lesions, causes turning towards the lesioned side. Mazindol-induced anorexia is antagonized by pretreatment with alpha-methyl-p-tyrosine or pimozide. Pimozide pretreatment prevents the rotation induced by Mazindol in rats with unilateral nigro-striatal lesions. The involvement of dopamine in the mechanism whereby Mazindol elicits anorexia and turning behaviour is discussed.

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