G L Ricchieri

University of Padova, Padua, Veneto, Italy

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Publications (10)30.65 Total impact

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    ABSTRACT: Neuropathological hallmarks of Alzheimer's disease (AD) are amyloid plaques and neurofibrillary tangles, containing betaA(42) peptide and tau protein, respectively. Amyloid plaques contain also glycosaminoglycans (GAGs). Whereas cerebrospinal fluid (CSF) levels of betaA(42) peptide and tau protein have been demonstrated as potential markers of Alzheimer's disease (AD), no data are available for GAGs. We determined (Elisa) tau and betaA(42) CSF levels, as well as serum antibodies to GAGs in 9 AD patients, and the values were analyzed in relation to age and severity of the disease. Beta-A42 and tau CSF levels were significantly reduced and increased, respectively, in AD patients when compared to controls, but they did not correlate with the severity of the disease. Despite their role in amyloidogenesis, we did not find evidence for the use of GAGs as diagnostic marker of AD.
    Journal of Neural Transmission 04/2002; 109(3):393-8. DOI:10.1007/s007020200031 · 2.40 Impact Factor
  • G L Ricchieri · G Pizzolato · M Fabbri · G M Patrassi · M T Sartori
    American Journal of Hematology 06/1996; 52(1):69-70. · 3.80 Impact Factor
  • American Journal of Hematology 05/1996; 52(1):69 - 70. DOI:10.1002/1096-8652(199605)52:1<69::AID-AJH2830520105>3.0.CO;2-O · 3.80 Impact Factor
  • Ulderico Freo · Gian Luigi Ricchieri · Harold W. Holloway · Timothy T. Soncrant
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    ABSTRACT: The time course and the relation to dose of regional cerebral metabolic rates for glucose (rCMRglc) were measured in awake male adult Fischer-344 rats after administration of quipazine, a serotonin 5-HT2-3 receptor agonist. rCMRglc was determined, using the quantitative autoradiographic [14C]deoxyglucose technique, in 92 brain regions at 30, 60, 90 and 120 min after quipazine 20 mg/kg i.p. and at 60 min after quipazine 5 mg/kg i.p. Peak metabolic effects were observed 60 min after quipazine 20 mg/kg i.p. when rCMRglc was significantly elevated in 27 (29%) brain regions (mean rise 17%). Quipazine increased rCMRglc in brain regions with high densities of 5-HT3 receptors (area postrema, olfactory tubercle, amygdala), in dopaminergic nuclei (substantia nigra pars compacta and pars reticulata) and terminal fields of their projections (zona incerta, subthalamic nucleus, preoptic magnocellular area, nucleus of facial nerve). The topographic distribution and direction of rCMRglc changes induced by quipazine are different from those produced by the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane and, consistent with the pharmacological and binding properties of quipazine, suggest a preferential activation of 5-HT3 receptors.
    Brain Research 02/1993; 600(2):249-56. DOI:10.1016/0006-8993(93)91380-B · 2.84 Impact Factor
  • G L Ricchieri · G Pizzolato · M Fabbri · S Ruggero · M Dam · L Battistin
    Advances in neurology 02/1993; 60:123-7. · 1.05 Impact Factor
  • M Dam · C Ori · G Pizzolato · G L Ricchieri · A Pellegrini · G P Giron · L Battistin
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    ABSTRACT: The autoradiographic 14C-2-deoxy-D-glucose method was used to determine local cerebral glucose utilization (LCGU) during propofol anesthesia and recovery in 52 regions of the rat brain. Control rats intravenously received 5 ml.kg-1.h-1 of the egg-oil-glycerol emulsion that constitutes the vehicle for propofol. Anesthetized animals received an iv bolus of propofol (20 mg/kg) followed by continuous infusion of the anesthetic at 12.5, 25, or 50 mg.kg-1.h-1 for 1 h prior to injection of 14C-2-deoxy-D-glucose and for the following 45 min. In addition, a fifth group of animals were studied immediately after awakening from a 20 mg/kg bolus of propofol as indicated by the first reappearance of head lift. All rats were spontaneously breathing room air throughout the experimental procedure. The general pattern of the cerebral metabolic response to propofol anesthesia was a dose-related, widespread depression of LCGU. At the three infusion rates of propofol tested, overall mean LCGU was reduced by 33%, 49%, and 55%, respectively, and significant decreases were observed in 60%, 85%, and 90% of the regions assayed. These effects were rapidly reversible, since in the recovery group, LCGU returned to near control values in the majority of the brain areas. Although all of the anatomofunctional systems (sensorimotor, extrapyramidal, limbic, and reticular) were involved, forebrain structures showed a greater sensitivity to the depressant action of propofol than did hindbrain regions.(ABSTRACT TRUNCATED AT 250 WORDS)
    Anesthesiology 10/1990; 73(3):499-505. DOI:10.1097/00000542-199009000-00021 · 5.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The time course and relation to dose of regional cerebral metabolic rates for glucose (rCMRglc) and of motor behavior were measured in awake male adult Fischer-344 rats after administration of meta-chlorophenylpiperazine (MCPP), a serotonin-1B receptor agonist. rCMRglc was determined, using the quantitative autoradiographic [14C]deoxyglucose technique, in 71 brain regions at 5, 15, 30 and 60 min after administration of MCPP 2.5 mg/kg i.p., and at 15 min after MCPP 25 and 40 mg/kg. The time course of performance on a rotating rod was measured periodically for 60 min after MCPP 2.5 mg/kg, a dose which impaired locomotion and reduced rCMRglc maximally at 15-30 min after its administration. At 15 min, rCMRglc declined significantly in 28 (40%) of the areas studied (mean decline 16%). Most regions affected were telencephalic or diencephalic, corresponding to the projection areas of serotonergic fibers arising from the raphe nuclei. After higher doses of MCPP, a behavioral serotonin syndrome was observed with both rCMRglc increases and decreases (25 mg/kg) or only rCMRglc increases (40 mg/kg). Whereas behavioral and metabolic activation induced by high doses of MCPP may result from stimulation at postsynaptic serotonin receptors, rCMRglc reductions and hypomotility produced by MCPP 2.5 mg/kg resemble the effects of serotonin receptor antagonists and suggest that, at this low dose, MCPP acts at modulatory serotonin autoreceptors to reduce endogenous serotonin release.
    Brain Research 04/1990; 511(2):209-16. DOI:10.1016/0006-8993(90)90163-6 · 2.84 Impact Factor
  • R de Caro · A Parenti · G Capitanio · C Ori · F Bracco · G L Ricchieri
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    ABSTRACT: A vascular malformation, consisting of a venous vessel bridgeing the right inferior petrosal sinus and the anterior spinal veins, was found in the posterior fossa. The vessel presented a ring-like course around the right trigeminal root, and it was parallel and dorsal to the basilar artery. The malformation was associated with cutaneous and hepatic angiomas and peri-osteal lipomas. It had been clinically silent for 52 years, when it thrombosed causing death. The authors think that, within a general mesenchymopatic state, this is a result of the persistence of an embryonal cerebral venous pattern.
    Acta Neurochirurgica 02/1990; 104(1-2):73-6. DOI:10.1007/BF01842898 · 1.77 Impact Factor
  • G. Pizzolato · M. Dam · N. Perlotto · G. L. Ricchieri · G. Ferlin · L. Battistin
    Acta Neurologica Scandinavica 03/1989; 79(3):265-265. DOI:10.1111/j.1600-0404.1989.tb03774.x · 2.40 Impact Factor
  • G L Ricchieri · T T Soncrant · H W Holloway · S I Rapoport
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    ABSTRACT: Local cerebral glucose utilization (LCGU) was measured, using the quantitative autoradiographic [14C]2-deoxy-D-glucose method, in 92 discrete brain regions of awake rats, at 1, 2, 3, or 4 h after administration of the serotonergic antagonist methiothepin 0.1 mg/kg IP. The drug produced a cataleptic behavior that peaked in intensity at 3 h after its administration. LCGU declined significantly in 35% of the 92 regions at one or more time points after methiothepin administration. No area of increased metabolism was found. The time-course of the decline in LCGU closely paralleled the intensity of catalepsy; the peak effect was at 3 h, when LCGU was significantly reduced in 32% of the regions examined (mean decline for all regions was 15%). Metabolic depression after methiothepin was most notable in the forebrain, where LCGU declined in many regions of the cerebral cortex, basal ganglia, and thalamus. Most of the regions affected by methiothepin possess a substantial number of serotonin receptors, although LCGU was also reduced in a few regions not primarily involved in serotonergic neurotransmission.
    Psychopharmacology 02/1987; 93(4):449-56. DOI:10.1007/BF00207234 · 3.88 Impact Factor

Publication Stats

110 Citations
30.65 Total Impact Points


  • 1990–1996
    • University of Padova
      Padua, Veneto, Italy
  • 1989–1993
    • It-Robotics
      Vicenza, Veneto, Italy
  • 1987–1993
    • National Institute on Aging
      • Laboratory of Neurosciences (LNS)
      Baltimore, Maryland, United States