title: Methylphenidate treatment increases Na(+), K (+)-ATPase activity in the cerebrum of young and adult rats.
abstract: Methylphenidate is a central nervous system stimulant used for the treatment of attention-deficit hyperactivity disorder. Na(+), K(+)-ATPase is a membrane-bound enzyme necessary to maintain neuronal excitability. Considering that methylphenidate effects on central nervous system metabolism are poorly known and that Na(+), K(+)-ATPase is essential to normal brain function, the purpose of this study was to evaluate the effect of this drug on Na(+), K(+)-ATPase activity in the cerebrum of young and adult rats. For acute administration, a single injection of methylphenidate (1.0, 2.0, or 10.0 mg/Kg) or saline was given to rats on postnatal day 25 or postnatal day 60, in the young and adult groups, respectively. For chronic administration, methylphenidate (1.0, 2.0, or 10.0 mg/Kg) or saline injections were given to young rats starting at postnatal day 25 once daily for 28 days. In adult rats, the same regimen was performed starting at postnatal day 60. Our results showed that acute methylphenidate administration increased Na(+), K(+)-ATPase activity in hippocampus, prefrontal cortex, and striatum of young and adult rats. In young rats, chronic administration of methylphenidate also enhanced Na(+), K(+)-ATPase activity in hippocampus and prefrontal cortex, but not in striatum. When tested in adult rats, Na(+), K(+)-ATPase activity was increased in all cerebral structures studied. The present findings suggest that increased Na(+), K(+)-ATPase activity may be associated with neuronal excitability caused by methylphenidate.
authors.affiliation: Laboratório de Neuroproteção e Doenças Metabólicas, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, CEP 90035-003, Porto Alegre, RS, Brazil.
authors.forename: Emilene B S
authors.initials: EB
authors.lastname: Scherer
authors.forename: Cristiane
authors.initials: C
authors.lastname: Matté
authors.forename: Andréa G K
authors.initials: AG
authors.lastname: Ferreira
authors.forename: Karin M
authors.initials: KM
authors.lastname: Gomes
authors.forename: Clarissa M
authors.initials: CM
authors.lastname: Comim
authors.forename: Cristiane
authors.initials: C
authors.lastname: Mattos
authors.forename: João
authors.initials: J
authors.lastname: Quevedo
authors.forename: Emilio L
authors.initials: EL
authors.lastname: Streck
authors.forename: Angela T S
authors.initials: AT
authors.lastname: Wyse
mesh_terms: D000375:Aging; D000818:Animals; D000697:Central Nervous System Stimulants / Q000008:administration & dosage / Q000494:pharmacology*; D054022:Cerebrum / Q000187:drug effects* / Q000201:enzymology* / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D008297:Male; D008774:Methylphenidate / Q000008:administration & dosage / Q000494:pharmacology*; D017397:Prefrontal Cortex / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013997:Time Factors
chemical_list: D000697:Central Nervous System Stimulants; D008774:Methylphenidate; D000254:Sodium-Potassium-Exchanging ATPase