Protein synthesis inhibition effects on dyskinesias induction

MARIANO SABORIDO; CELIA LARRAMENDY; IRENE TARAVINI; GUSTAVO MURER; OSCAR GERSHANIK

Tandil, Argentina

Congreso; Cuadragésima Reunión Anual de la Sociedad Argentina de Farmacología Experimental; 2008

Sociedad Argentina de Farmacología Experimental (SAFE)

<!-- /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin:0cm; margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-fareast-font-family:"Times New Roman";} @page Section1 {size:612.0pt 792.0pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:36.0pt; mso-footer-margin:36.0pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> Dyskinesias are one of the major limiting side effects encountered in the treatment of Parkinson´s disease. To demonstrate that protein synthesis is required for the priming effect of dopamine agonists on the generation of dyskinesias, 22-gauge stainless steel cannulas were implanted hemilaterally in the striatum.  Anisomycin (160µg/1.6µl) or vehicle were infused 15 min before apomorphine (0.025mg/kg) or vehicle once every  48 h a total of three times (priming). Forty eight hours later, all groups received 0.05mg/kg apomorphine. After apomorphine administration contralateral rotations and dyskinesias were tested. Twenty minutes after apomorphine akinesia of the contralateral forepaw was also tested by means of the cylinder test. Our results suggests that the administration of anisomycin during priming with apomorphine diminishes dyskinesia severity induced by a new challenge with apomorphine. This preliminary data indicates that protein synthesis could be necessary for the plastic changes that occur in response to dopamine agonists and that give origin to dyskinesia in an animal model of parkinsonism.