Compounds acting at the endocannabinoid and/or endovanilloid systems reduce hyperkinesia in a rat model of Huntington's disease (Articolo in rivista)

Type

• Articolo in rivista (Classe)
• Prodotto della ricerca (Classe)

Label

• Compounds acting at the endocannabinoid and/or endovanilloid systems reduce hyperkinesia in a rat model of Huntington's disease (Articolo in rivista) (literal)

Anno

• 2003-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

• 10.1046/j.1471-4159.2003.01595.x (literal)

Alternative label

• Lastres-Becker I.; de Miguel R.; De Petrocellis L.; Makriyannis A.; Di Marzo V. and Fernández-Ruiz J. (2003)
  Compounds acting at the endocannabinoid and/or endovanilloid systems reduce hyperkinesia in a rat model of Huntington's disease
  in Journal of neurochemistry; Blackwell Publishing, Oxford (Regno Unito)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Lastres-Becker I.; de Miguel R.; De Petrocellis L.; Makriyannis A.; Di Marzo V. and Fernández-Ruiz J. (literal)

Pagina inizio

• 1097 (literal)

Pagina fine

• 1109 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 84 (literal)

Rivista

• Journal of neurochemistry (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

• IF 2002: 4,969. Settore disciplinare Biochimica e Biologia molecolare (categorie ISI-CRUI). La rivista è nella fascia di eccellenza del settore (da 4,50 a 36,28). IF ricalcolato in base al rango: 0,827. ImmediacyIndex 0,53, Cit Half-Life 6,3. (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

• 5 (literal)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• 1. Univ Complutense, Dept Bioquim & Biol Mol, Fac Med, E-28040 Madrid, Spain 2. CNR, Endocannabinoid Res Grp, Ist Cibernetica, Naples, Italy 3. CNR, Endocannabinoid Res Grp, Ist Chim Biomol, Naples, Italy 4. Univ Connecticut, Dept Pharmaceut Sci, Ctr Drug Discovery, Storrs, CT USA 5. Univ Connecticut, Dept Mol & Cell Biol, Ctr Drug Discovery, Storrs, CT 06269 USA (literal)

Titolo

• Compounds acting at the endocannabinoid and/or endovanilloid systems reduce hyperkinesia in a rat model of Huntington's disease (literal)

Abstract

• We have recently reported that the administration of AM404, an inhibitor of the endocannabinoid re-uptake process, which also has affinity for the vanilloid VR1 receptors, is able to reduce hyperkinesia, and causes recovery from neurochemical deficits, in a rat model of Huntington's disease (HD) generated by bilateral intrastriatal injections of 3-nitropropionic acid (3NP). In the present study, we wanted to explore the mechanism(s) by which AM404 produces its antihyperkinetic effect in 3NP-lesioned rats by employing several experimental approaches. First, we tried to block the effects of AM404 with selective antagonists for the CB1 or VR1 receptors, i.e. SR141716A and capsazepine, respectively. We found that the reduction caused by AM404 of the increased ambulation exhibited by 3NP-lesioned rats in the open-field test was reversed when the animals had been pre-treated with capsazepine but not with SR141716A, thus suggesting a major role of VR1 receptors in the antihyperkinetic effects of AM404. However, despite the lack of behavioral effects of the CB1 receptor antagonist, the pretreatment with this compound abolished the recovery of neurochemical [gamma-aminobutyric acid (GABA) and dopamine] deficits in the caudate- putamen caused by AM404, as also did capsazepine. In a second group of studies, we wanted to explore the potential antihyperkinetic effects of various compounds which, compared to AM404, exhibit more selectivity for either the endovanilloid or the endocannabinoid systems. First, we tested VDM11 or AM374, two selective inhibitors or the endocannabinoid re-uptake or hydrolysis, respectively. Both compounds were mostly unable to reduce hyperkinesia in 3NP-lesioned rats, although VDM11 produced a certain motor depression, and AM374 exhibited a trend to stimulate ambulation, in control rats. We also tested the effects of selective direct agonists for VR1 (capsaicin) or CB1 (CP55,940) receptors. Capsaicin exhibited a strong antihyperkinetic activity and, moreover, was able to attenuate the reductions in dopamine and GABA transmission provoked by the 3NP lesion, whereas CP55,940 had also antihyperkinetic activity but was unable to cause recovery of either dopamine or GABA deficits in the basal ganglia. In summary, our data indicate a major role for VR1 receptors, as compared to CB1 receptors, in the antihyperkinetic effects and the recovery of neurochemical deficits caused in 3NP-lesioned rats by compounds that activate both CB1 and VR1 receptors, either directly or via manipulation of the levels of endogenous agonists. (literal)

Editore

• Blackwell Publishing (Editore)

Prodotto di

• Istituto di cibernetica \"Edoardo Caianiello\" (ISASI) (Istituto)
• Istituto di chimica biomolecolare (ICB) (Istituto)

Autore CNR

• VINCENZO DI MARZO (Unità di personale interno)
• LUCIANO DE PETROCELLIS (Persona)

Insieme di parole chiave

• Keywords of "Compounds acting at the endocannabinoid and/or endovanilloid systems reduce hyperkinesia in a rat model of Huntington's disease" (Insieme di parole chiave)

Incoming links:

Prodotto

• Istituto di cibernetica \"Edoardo Caianiello\" (ISASI) (Istituto)
• Istituto di chimica biomolecolare (ICB) (Istituto)

Autore CNR di

• VINCENZO DI MARZO (Unità di personale interno)
• LUCIANO DE PETROCELLIS (Persona)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Journal of neurochemistry (Rivista)

Editore di

• Blackwell Publishing (Editore)

Insieme di parole chiave di

• Keywords of "Compounds acting at the endocannabinoid and/or endovanilloid systems reduce hyperkinesia in a rat model of Huntington's disease" (Insieme di parole chiave)