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Methylphenidate treatment affects mitogen-activated protein kinase activation in the striatum of young rats

Published online by Cambridge University Press:  07 March 2013

Clarissa M. Comim
Affiliation:
Laboratory of Neurosciences and National Institute for Translational Medicine (INCT-TM), Postgradute Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil
Josimar G. Pereira
Affiliation:
Laboratory of Neurosciences and National Institute for Translational Medicine (INCT-TM), Postgradute Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil
Sandro J. Ribeiro
Affiliation:
Laboratory of Neurosciences and National Institute for Translational Medicine (INCT-TM), Postgradute Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil
João Quevedo
Affiliation:
Laboratory of Neurosciences and National Institute for Translational Medicine (INCT-TM), Postgradute Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil
Carina R. Boeck*
Affiliation:
Laboratory of Neurosciences and National Institute for Translational Medicine (INCT-TM), Postgradute Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil
*
Dr. Carina R. Boeck, Laboratório de Neurociências, PPGCS, UNASAU, Universidade do Extremo Sul Catarinense, Av. Universitária - 1106, Bairro Universitária, 88806-000 Criciúma, SC, Brazil. Fax: +55 48 3431 2758; E-mail bcr@unesc.net

Abstract

Objective

Methylphenidate (MPD) is a drug prescribed for the treatment of attention deficit/hyperactivity disorder and its therapeutic effect is attributed to the inhibition of dopamine.

Methods

Young male Wistar rats were administered MPD (1, 2, 5, or 10 mg/kg) once a day or an intraperitoneal injection of saline for 28 days (chronic treatment) or for 1 day (acute treatment). Two hours after the last administration the animals were decapitated and their striatum was dissected.

Results

In this work, we show that continued treatment with MPD is capable of modifying the levels of phosphorylation of proteins JNK1/2 (c-Jun amino-terminal kinases 1 and 2) and ERK1/2 (extracellular signal-regulated kinases 1 and 2). Whereas the level of phosphorylation of protein ERK increased significantly, that of proteins JNK1/2 diminished.

Conclusion

The alteration in the level of activation of mitogen-activated protein kinases can be a molecular mechanism through which MPD exerts its therapeutic effect.

Type
Short Communications
Copyright
Copyright © Scandinavian College of Neuropsychopharmacology 2013 

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