Cognitive Imapirment in an experimental model of Parkinson´s Disease

MACARENA LORENA HERRERA; ROMINA DEZA-PONZIO; OSVALDO M. BASMADJIAN; VICTORIA B. OCCHIEPPO; VICTOR A MOLINA; MARÍA JOSÉ BELLINI; CLAUDIA B. HEREÑÚ

Florianópolis

Congreso; International Neurotoxicology Association and Neurotoxicity Society Meeting 2017; 2017

BACKGROUND: Parkinson´s disease is a neurodegenerative disorder that results from aprogressive dopaminergic neuronal loss. It is considered a multifactorial condition due tothe multiplicity of symptoms experienced by patients. While this condition is known for itscharacteristic motor deficits, patients also have wide variety non-motor symptoms amongthem, 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, theprogression of working memory deficits and its correlation with the loss of dopaminergicneurons.METHODS: Adult male Wistar rats were stereotaxically injected with the neurotoxin6OHDA 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 thebehavioral tasks after 7, 14, 20 and 28 days. A group of animals were tested in the workingmemory task Y-maze and motor function was characterized using locomotor activity withamphetamine administration, stick and hot plate tests. After that, the rats were perfused andtheir brain processed for immunohistochemical of tyrosine hydroxylase (TH) in thesubstantia nigra (SN), DLS, dorsal hippocampus (CA1) and prefrontal cortex (PFC).RESULTS: Working memory deficits were observed in 6OHDA rats compared to Vehiclerats after 20 and 28 days of neurodegeneration (p