RESUMEN
Although dopamine replacement therapy with L-DOPA in Parkinson's disease initially reduces motor symptoms, its chronic use often leads to the development of abnormal involuntary movements known as L-DOPA-induced dyskinesia. Increasingly, research has indicated that non-dopaminergic neurons gain function in the parkinsonian brain, taking up and converting L-DOPA to dopamine and releasing it as a "false neurotransmitter". Although less explored, promiscuity between monoamine transporters may also modulate these processes. Therefore, in order to examine the differential roles of monoamine transporters in L-DOPA's behavioral effects, three tricyclic antidepressants (TCA) with graded affinity for serotonin (SERT) vs. norepinephrine (NET) transporters were tested in hemi-parkinsonian rats: clomipramine (SERT>NET), amitriptyline (SERT=NET), and desipramine (SERTAsunto(s)
Antidepresivos Tricíclicos/uso terapéutico
, Discinesias/tratamiento farmacológico
, Levodopa/uso terapéutico
, Trastornos Parkinsonianos/tratamiento farmacológico
, Animales
, Cuerpo Estriado/metabolismo
, Dopamina/metabolismo
, Discinesias/fisiopatología
, Levodopa/administración & dosificación
, Masculino
, Proteínas de Transporte de Noradrenalina a través de la Membrana Plasmática/efectos de los fármacos
, Oxidopamina/metabolismo
, Trastornos Parkinsonianos/fisiopatología
, Ratas
, Ratas Sprague-Dawley
, Proteínas de Transporte de Serotonina en la Membrana Plasmática/efectos de los fármacos