Evidence for the involvement of the adenosine A2A receptor in the lowered susceptibility to pentylenetetrazol-induced seizures produced in mice by long-term treatment with caffeine

Uloženo v:
Podrobná bibliografie
Název: Evidence for the involvement of the adenosine A2A receptor in the lowered susceptibility to pentylenetetrazol-induced seizures produced in mice by long-term treatment with caffeine
Autoři: El Yacoubi, Malika, Ledent, Catherine, Parmentier, Marc, Costentin, Jean, Vaugeois, Jean-Marie
Přispěvatelé: Neuropsycho-pharmacologie expérimentale, Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Université libre de Bruxelles (ULB)
Zdroj: Neuropharmacology. 55:35-40
Informace o vydavateli: Elsevier BV, 2008.
Rok vydání: 2008
Témata: Male, 0301 basic medicine, Time Factors, Receptor, Adenosine A2A, Phosphodiesterase Inhibitors, Knockout, Adenosine A2A -- deficiency, Adenosine A2A receptor, Reaction Time -- genetics, Pentylenetetrazol, Dose-Response Relationship, Phosphodiesterase Inhibitors -- administration & dosage, Mice, 03 medical and health sciences, 0302 clinical medicine, Seizures, Caffeine, Reaction Time, Animals, Reaction Time -- drug effects, Seizures -- chemically induced, Mice, Knockout, Analysis of Variance, Dose-Response Relationship, Drug, Animal, Sciences bio-médicales et agricoles, Adenosine A2A -- physiology, Seizure, 3. Good health, Disease Models, Animal, Kindling, Disease Models, Pentylenetetrazole, Disease Susceptibility, Drug, Caffeine -- administration & dosage, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Seizures -- drug therapy, Receptor, Knockout mice
Popis: Long-term caffeine intake has been reported to decrease the susceptibility to convulsants in mice. Occurrence of seizures following long-term oral administration of caffeine (0.3g/l) was investigated using adenosine A(2A) receptor knockout (A(2A)R KO) and control (A(2A)R WT) mice. Clonic seizures induced by acute pentylenetetrazol (PTZ, 50mg/kg i.p.) were significantly attenuated in adenosine A(2A)R KO mice drinking only water and reduced by a 14-day caffeine treatment in adenosine A(2A)R WT mice. In addition we showed a protecting effect of a 21-day caffeine treatment in A(2A)R WT mice against kindled seizures induced by PTZ in an increasing dose schedule. Summing up, these protective effects against PTZ-induced seizures occurring when adenosine A(2A)R is absent or chronically blocked by a relevant dose of caffeine may be related to a decreased neuronal excitability.
Druh dokumentu: Article
Popis souboru: 1 full-text file(s): application/pdf
Jazyk: English
ISSN: 0028-3908
DOI: 10.1016/j.neuropharm.2008.04.007
Přístupová URL adresa: https://pubmed.ncbi.nlm.nih.gov/18486156
https://difusion.ulb.ac.be/vufind/Record/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/52304/Details
https://pubmed.ncbi.nlm.nih.gov/18486156/
https://www.ncbi.nlm.nih.gov/pubmed/18486156
https://core.ac.uk/display/8852166
https://www.sciencedirect.com/science/article/pii/S0028390808001044
Rights: Elsevier TDM
Přístupové číslo: edsair.doi.dedup.....24592b11a8b24d41f6330632b6f548e5
Databáze: OpenAIRE
Popis
Abstrakt:Long-term caffeine intake has been reported to decrease the susceptibility to convulsants in mice. Occurrence of seizures following long-term oral administration of caffeine (0.3g/l) was investigated using adenosine A(2A) receptor knockout (A(2A)R KO) and control (A(2A)R WT) mice. Clonic seizures induced by acute pentylenetetrazol (PTZ, 50mg/kg i.p.) were significantly attenuated in adenosine A(2A)R KO mice drinking only water and reduced by a 14-day caffeine treatment in adenosine A(2A)R WT mice. In addition we showed a protecting effect of a 21-day caffeine treatment in A(2A)R WT mice against kindled seizures induced by PTZ in an increasing dose schedule. Summing up, these protective effects against PTZ-induced seizures occurring when adenosine A(2A)R is absent or chronically blocked by a relevant dose of caffeine may be related to a decreased neuronal excitability.
ISSN:00283908
DOI:10.1016/j.neuropharm.2008.04.007