Lesion of the subthalamic nucleus reverses motor deficits but not death of nigrostriatal dopaminergic neurons in a rat 6-hydroxydopamine-lesion model of Parkinson's disease

• Autor(a) principal: Rizélio, Vanessa
• Data de Publicação: 2010
• Outros Autores: Szawka, Raphael Escorsim, Xavier, Leder Leal, Achaval-Elena, Matilde, Soster, Paula Rigon da Luz, Saur, Lisiani, Matheussi, Francesca, Delattre, Ana Márcia, Franci, Janete Aparecida Anselmo, Meneses, Murilo Sousa de, Ferraz, Anete Curte
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/28252
• topic: Doença de Parkinson; Substância negra; Núcleo subtalâmico; Oxidopamina; Subthalamic nucleus; Parkinson’s disease; Substantia nigra pars compacta; 6-Hydroxydopamine; Tyrosine hydroxylase immunohistochemistry

The objective of the present study was to determine whether lesion of the subthalamic nucleus (STN) promoted by N-methyl- D-aspartate (NMDA) would rescue nigrostriatal dopaminergic neurons after unilateral 6-hydroxydopamine (6-OHDA) injection into the medial forebrain bundle (MFB). Initially, 16 μg 6-OHDA (6-OHDA group) or vehicle (artificial cerebrospinal fluid - aCSF; Sham group) was infused into the right MFB of adult male Wistar rats. Fifteen days after surgery, the 6-OHDA and Sham groups were randomly subdivided and received ipsilateral injection of either 60 mM NMDA or aCSF in the right STN. Additionally, a control group was not submitted to stereotaxic surgery. Five groups of rats were studied: 6-OHDA/NMDA, 6-OHDA/Sham, Sham/ NMDA, Sham/Sham, and control. Fourteen days after injection of 6-OHDA, rats were submitted to the rotational test induced by apomorphine (0.1 mg/kg, ip) and to the open-field test. The same tests were performed again 14 days after NMDA-induced lesion of the STN. The STN lesion reduced the contralateral turns induced by apomorphine and blocked the progression of motor impairment in the open-field test in 6-OHDA-treated rats. However, lesion of the STN did not prevent the reduction of striatal concentrations of dopamine and metabolites or the number of nigrostriatal dopaminergic neurons after 6-OHDA lesion. Therefore, STN lesion is able to reverse motor deficits after severe 6-OHDA-induced lesion of the nigrostriatal pathway, but does not protect or rescue dopaminergic neurons in the substantia nigra pars compacta.