IFEC   20925
INSTITUTO DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Cognitive Imapirment in an experimental model of Parkinson´s Disease
Autor/es:
OSVALDO M. BASMADJIAN; MARÍA JOSÉ BELLINI; ROMINA DEZA-PONZIO; VICTOR A MOLINA; MACARENA LORENA HERRERA; VICTORIA B. OCCHIEPPO; CLAUDIA HEREÑÚ
Lugar:
Florianópolis, Santa Catarina
Reunión:
Congreso; International Neurotoxicology Association and Neurotoxicity Society Meeting 2017; 2017
Institución organizadora:
International Neurotoxicology Association and Neurotoxicity Society
Resumen:
BACKGROUND: Parkinson´s disease is a neurodegenerative disorder that results from a progressive dopaminergic neuronal loss. It is considered a multifactorial condition due to the multiplicity of symptoms experienced by patients. While this condition is known for its characteristic motor deficits, patients also have wide variety non-motor symptoms among them, impaired learning and memory deficits which severely affect their quality of life. These non-motor symptoms result from the dysfunction of interconnected systems, including the striatum, the neocortex and the hippocampus.OBJECTIVES: To determine, in an experimental model of the neuropathology, the progression of working memory deficits and its correlation with the loss of dopaminergic neurons.METHODS: Adult male Wistar rats were stereotaxically injected with the neurotoxin 6OHDA in dorsal lateral striatum (DLS) or with the control solution of ascorbic saline. Independent groups of animals (12-15 rats per group) were tested only once in the behavioral tasks after 7, 14, 20 and 28 days. A group of animals were tested in the working memory task Y-maze and motor function was characterized using locomotor activity with amphetamine administration, stick and hot plate tests. After that, the rats were perfused and their brain processed for immunohistochemical of tyrosine hydroxylase (TH) in the substantia nigra (SN), DLS, dorsal hippocampus (CA1) and prefrontal cortex (PFC).RESULTS: Working memory deficits were observed in 6OHDA rats compared to Vehicle rats after 20 and 28 days of neurodegeneration (p