Pavone F

References (11)

Title : M2 Receptors Exert Analgesic Action on DRG Sensory Neurons by Negatively Modulating VR1 Activity - De Angelis_2014_J.Cell.Physiol_229_783
Author(s) : De Angelis F , Marinelli S , Fioretti B , Catacuzzeno L , Franciolini F , Pavone F , Tata AM
Ref : Journal of Cellular Physiology , 229 :783 , 2014
Abstract : The peripheral application of the M2 cholinergic agonist arecaidine on sensory nerve endings shows anti-nociceptive properties. In this work, we analyze in vitro, the mechanisms downstream M2 receptor activation causing the analgesic effects, and in vivo the effects produced by M2 agonist arecaidine administration on nociceptive responses in a murine model of nerve growth factor (NGF)-induced pain. Cultured DRG neurons treated with arecaidine showed a decreased level of VR1 and SP transcripts. Conversely, we found an increased expression of VR1 and SP transcripts in DRG from M2/M4(-/-) mice compared to WT and M1(-/-) mice, confirming the inhibitory effect in particular of M2 receptors on SP and VR1 expression. Patch-clamp experiments in the whole-cell configuration showed that arecaidine treatment caused a reduction of the fraction of capsaicin-responsive cells, without altering the mean capsaicin-activated current in responsive cells. We also demonstrated that arecaidine prevents PKC translocation to the plasma membrane after inflammatory agent stimulation, mainly in medium-small sensory neurons. Finally, in mice, we have observed that intraperitoneal injection of arecaidine reduces VR1 expression blocking hyperalgesia and allodynia caused by NGF intraplantar administration. In conclusion, our data demonstrate that in vivo M2 receptor activation induces desensitization to mechanical and heat stimuli by a down-regulation of VR1 expression and by the inhibition of PKC activity hindering its translocation to the plasma membrane, as suggested by in vitro experiments. J. Cell. Physiol. 229: 783-790, 2014. (c) 2013 Wiley Periodicals, Inc.
ESTHER : De Angelis_2014_J.Cell.Physiol_229_783
PubMedSearch : De Angelis_2014_J.Cell.Physiol_229_783
PubMedID: 24166293

Title : Central injection of botulinum neurotoxins: behavioural effects in mice - Luvisetto_2004_Behav.Pharmacol_15_233
Author(s) : Luvisetto S , Marinelli S , Rossetto O , Montecucco C , Pavone F
Ref : Behav Pharmacol , 15 :233 , 2004
Abstract : Strains of Clostridium botulinum produce seven antigenically distinct botulinum neurotoxins (BoNTs) designated as serotypes A-G. All serotypes interfere with neural transmission by blocking the release of acetylcholine in cholinergic neurons. They cleave specific sites on proteins of the SNARE [soluble n-ethylmaleimide-sensitive factor (NSF) attachment protein receptor] complex, which play a key role in neuroexocytosis. This study assessed the behavioural effects due to central administration of BoNTs in mice. CD1 mice were injected intracerebroventricularly (icv) with sub-lethal doses of BoNT/A or /B and their behavioural responses in conditioning of active avoidance, object recognition test and pharmacologically induced locomotor activity were tested. Compared to control mice, BoNT-treated mice showed: (1) a reduced capacity to discriminate a novel object within a familiar environment; (2) an enhanced stimulant effect by scopolamine and a depressant effect by oxotremorine on locomotor activity. In contrast, central injection of BoNTs did not alter active avoidance acquisition. These results suggest an in vivo functional alteration due to the action of BoNTs directly administered into the central nervous system. The present data demonstrate that BoNTs may represent an analytical tool for studying the functional role of cholinergic neurons.
ESTHER : Luvisetto_2004_Behav.Pharmacol_15_233
PubMedSearch : Luvisetto_2004_Behav.Pharmacol_15_233
PubMedID: 15187581

Title : Toxicity of botulinum neurotoxins in central nervous system of mice - Luvisetto_2003_Toxicon_41_475
Author(s) : Luvisetto S , Rossetto O , Montecucco C , Pavone F
Ref : Toxicon , 41 :475 , 2003
Abstract : Botulinum neurotoxins (BoNTs) act specifically on cholinergic nerve terminals, where they cause a sustained block of acetylcholine release, and therefore they are powerful tools to study the role of cholinergic neurons in neuronal processes. Peripheral effects of BoNTs are widely documented while central effects have not been studied. Here, we report for the first time on the central toxicity of BoNT serotypes A and B following their direct intracerebroventricular (icv) injection in CD1 mice. The LD50 values were found to be in the range 0.5-1.0 x 10(-6)mg/kg. We recorded the following signs preceding animal death: piloerection and weight decrease appear first, followed by temperature decrease, eyelid closure, loss of sensorimotor reflexes, dehydration, dyspnea. Mice died of heart or respiratory failure. The surviving mice recovered completely within 4-6 days and regained the initial healthy conditions. At sub-lethal doses, the same clinical signs appear in a lighter form and with a longer time course.
ESTHER : Luvisetto_2003_Toxicon_41_475
PubMedSearch : Luvisetto_2003_Toxicon_41_475
PubMedID: 12657317

Title : Effects of the novel acetylcholinesterase inhibitor N-octyl-1,2,3, 4- tetrahydro-9-aminoacridine on locomotor activity and avoidance learning in mice - Capone_1999_Neurobiol.Learn.Mem_71_301
Author(s) : Capone F , Oliverio A , Pomponi M , Marta M , Gatta F , Pavone F
Ref : Neurobiol Learn Mem , 71 :301 , 1999
Abstract : The acetylcholinesterase reversible inhibitor N-octyl-1,2,3, 4-tetrahydro-9-aminoacridine (THA-C8) is a new synthesized derivative of tacrine (THA) characterized by an alkyl chain in the molecular structure which ameliorates the penetrability of the compound into the central nervous system. THA-C8 (0.1-5 mg/kg) significantly reduced spontaneous locomotor activity in CD1 mice at a dose of 3 mg/kg. Moreover, THA-C8 (0.2-2 mg/kg) significantly improved shuttle-box avoidance acquisition at doses (0.25, 0.3, 1 mg/kg) not affecting locomotion and that are much lower than the doses reported to be effective for THA in animal models. From the data reported it seems that the new compound could be interesting for therapeutic purposes.
ESTHER : Capone_1999_Neurobiol.Learn.Mem_71_301
PubMedSearch : Capone_1999_Neurobiol.Learn.Mem_71_301
PubMedID: 10196108

Title : Shuttle-box avoidance learning in mice: improvement by combined glucose and tacrine - Pavone_1998_Neurobiol.Learn.Mem_69_204
Author(s) : Pavone F , Capone F , Battaglia M , Sansone M
Ref : Neurobiol Learn Mem , 69 :204 , 1998
Abstract : Glucose and the acetylcholinesterase inhibitor tacrine were tested, alone and in combination, in mice of the CD-1 strain subjected to five daily shuttle-box training sessions. Pretraining intraperitoneal administration of glucose alone (50-400 mg/kg) had no significant effect, while tacrine alone (0.5-3 mg/kg) improved avoidance acquisition at the dose of 2 mg/kg only. Significant avoidance learning improvements were instead produced by 50 or 100 mg/kg glucose combined with 0.5 or 1 mg/kg tacrine. The effects on shuttle-box avoidance acquisition produced by glucose combined with a cholinomimetic agent support the hypothesis that cholinergic mechanisms may be involved in the action of glucose on learning and memory. However, the main finding of the present study is related to the enhancement by glucose of the learning improving action of a drug clinically used as cognitive enhancer.
ESTHER : Pavone_1998_Neurobiol.Learn.Mem_69_204
PubMedSearch : Pavone_1998_Neurobiol.Learn.Mem_69_204
PubMedID: 9619996

Title : Studies on a new series of THA analogues: effects of the aromatic residues that line the gorge of AChE - Pomponi_1997_FEBS.Lett_409_155
Author(s) : Pomponi M , Marta M , Colella A , Sacchi S , Patamia M , Gatta F , Capone F , Oliverio A , Pavone F
Ref : FEBS Letters , 409 :155 , 1997
Abstract : A series of N-monoalkylsubstituted 1,2,3,4-tetrahydro-9-aminoacridines have been prepared after modelling simulation of the AChE-inhibitor complex. Molecular modelling has predicted a number of hydrophobic residues to be involved in the catalytic mechanism of this interaction between the binding sites of AChE and this series of aminoacridines. In these compounds the acridine moiety becomes sandwiched between the rings of PHE330 and TRP84. In particular, the alkyl chain shows the important role of aromatic groups as binding sites. Their in vitro inhibitory properties (enzyme from Electrophorus electricus) confirm the aromatic groups as a general and significant characteristic of the mechanism of AChE inhibition.
ESTHER : Pomponi_1997_FEBS.Lett_409_155
PubMedSearch : Pomponi_1997_FEBS.Lett_409_155
PubMedID: 9202137

Title : Prevention of amitriptyline-induced avoidance impairment by tacrine in mice - Pavone_1997_Behav.Brain.Res_89_229
Author(s) : Pavone F , Battaglia M , Sansone M
Ref : Behavioural Brain Research , 89 :229 , 1997
Abstract : The effects of two cognition enhancers on avoidance impairment induced by the tricyclic antidepressant amitriptyline were assessed during shuttle-box avoidance acquisition and in previously trained mice of the DBA/2 strain. The nootropic agent piracetam (50, 100 or 200 mg/kg, i.p.) had slight or no effect in mice receiving amitriptyline (5 or 10 mg/kg, i.p.). Conversely, the acetylcholinesterase inhibitor tacrine (0.5, 1, 2 or 3 mg/kg, i.p.) prevented the avoidance impairment induced by 5 mg/kg amitriptyline on shuttle-box avoidance acquisition as well as on a previously learned avoidance response. The avoidance disrupting action produced by 10 mg/kg of the antidepressant drug was not affected by the anticholinesterase drug. The preventing action of tacrine seems specifically related to the avoidance impairment induced by amitriptyline, since the acetylcholinesterase inhibitor did not reduce, but enhanced the avoidance impairing action of the neuroleptic chlorpromazine. Taken together, the results indicate that amitriptyline-induced avoidance impairment, and the related preventing action of tacrine, may be ascribed to drug effects on the performance of the avoidance response, rather than to interferences with learning processes.
ESTHER : Pavone_1997_Behav.Brain.Res_89_229
PubMedSearch : Pavone_1997_Behav.Brain.Res_89_229
PubMedID: 9475630

Title : Enhancement by nifedipine of cholinergic-induced depression of locomotor activity in mice - Sansone_1995_Funct.Neurol_10_163
Author(s) : Sansone M , Battaglia M , Pavone F
Ref : Functional Neurology , 10 :163 , 1995
Abstract : The dihydropyridine calcium channel blocker nifedipine did not affect spontaneous locomotor activity in mice when given alone but enhanced the depressant effects of the muscarinic receptor agonist oxotremorine and of the acetylcholinesterase inhibitor physostigmine. Such a behavioral depression might be due to neuronal changes induced by central calcium channel blockade combined with cholinergic activation. However, an involvement of hemodynamic factors, related to peripheral vasodilatation, cannot be excluded as locomotor depressant effects were also exerted by combinations of the two cholinomimetic agents with hydralazine, a non-calcium antagonist vasodilator.
ESTHER : Sansone_1995_Funct.Neurol_10_163
PubMedSearch : Sansone_1995_Funct.Neurol_10_163
PubMedID: 8749042

Title : Phosphatidylserine administration during postnatal development improves memory in adult mice - Fagioli_1989_Neurosci.Lett_101_229
Author(s) : Fagioli S , Castellano C , Oliverio A , Pavone F , Populin R , Toffano G
Ref : Neuroscience Letters , 101 :229 , 1989
Abstract : Postnatal administration of an aqueous suspension of phosphatidylserine (BC-PS) to C57BL/6 mice resulted in improvement of memory processes in adulthood, as assessed in a passive avoidance task. These findings are discussed in terms of the effects of BC-PS on cholinergic mechanisms and of cholinergic patterns of this inbred strain.
ESTHER : Fagioli_1989_Neurosci.Lett_101_229
PubMedSearch : Fagioli_1989_Neurosci.Lett_101_229
PubMedID: 2771168

Title : New analogs of physostigmine: alternative drugs for Alzheimer's disease? - Marta_1988_Life.Sci_43_1921
Author(s) : Marta M , Castellano C , Oliverio A , Pavone F , Pagella PG , Brufani M , Pomponi M
Ref : Life Sciences , 43 :1921 , 1988
Abstract : The synthesis of a series of physostigmine analogs, in which the methylcarbamyl group has been substituted with monoalkylcarbamyl, dimethyl- and diethylcarbamyl groups, is reported. These compounds were prepared with the aim of investigating their possible therapeutic effects in the treatment of Alzheimer's type dementia. The new analogs of physostigmine are inhibitors of acetylcholinesterase from Electroforus electricus, with a value of the reactivation constant, k3 smaller than the one of physostigmine. The percentage of anticholinesterase activity in vitro and in vivo, the acute toxicity and some behavioural effects were also evaluated for selected derivatives. The reactivation constant, in vitro, supports the view that the derivatives described would be more suitable for therapeutic use than physostigmine.
ESTHER : Marta_1988_Life.Sci_43_1921
PubMedSearch : Marta_1988_Life.Sci_43_1921
PubMedID: 3200115

Title : A long-lasting cholinesterase inhibitor affecting neural and behavioral processes - Brufani_1987_Pharmacol.Biochem.Behav_26_625
Author(s) : Brufani M , Castellano C , Marta M , Oliverio A , Pagella PG , Pavone F , Pomponi M , Rugarli PL
Ref : Pharmacol Biochem Behav , 26 :625 , 1987
Abstract : A series of analogues of physostigmine were prepared with the aim of investigating their inhibitory effects on acetylcholinesterase in the treatment of Alzheimer's disease. One of the isomers prepared was evaluated for its anticholinesterase activity in vivo, acute toxicity, and some behavioral effects. This compound was a competitive inhibitor of the enzyme and was found to antagonize the stimulating effect produced by scopolamine on locomotor activity and to facilitate memory consolidation.
ESTHER : Brufani_1987_Pharmacol.Biochem.Behav_26_625
PubMedSearch : Brufani_1987_Pharmacol.Biochem.Behav_26_625
PubMedID: 3575379