Estudo da participação do hipocampo e da via nigro-estriatal na memória espacial e com dica visual em ratos

Abstract

Abstract: The aim of the present study was to test if the nigrostriatal pathway is an essential component for a water maze cued task learning and if it works independently of the hippocampal memory system. This hypothesis was tested using an animal model of Parkinson’s disease in which male Wistar rats were lesioned in the substantia nigra pars compacta (SNc) by the intranigral infusion of 1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP), thus causing a partial depletion of striatal dopamine. SNc-Iesioned and sham-operated animals were implanted bilaterally with guide cannulae above the dorsal hippocampus in order to be tested after the administration of 0.4 µl 2% lidocaine or saline into this structure. The animals were tested in a spatial or in a cued version of the water maze, memory tasks previously reported to model hippocampal-dependent spatial/relational and striatal-dependent S-R learning, respectively. Hippocampal inactivation, but not SNc lesion, impaired learning and memory in the spatial version of the water maze. An opposite situation was observed with the cued version. No significant interaction was observed between the Snc lesion and hippocampal inactivation conditions affecting scores in the spatial or in the cued version of the water maze. These results suggest that the nigrostriatal pathway is an essential part of the memory system that processes S-R learning and that it works independently of the hippocampal memory system that processes spatial/relational memories.

Abstract: The bilateral intranigral infusion of 1 µmol l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) in adult male Wistar rats caused a specific and partial loss of substantia nigra pars compacta (SNpc) dopaminergic neurons, a partial depletion of striatal dopamine (DA), and a deficit in learning the cued version of the water maze. This deficit was reversed by pretraining the SNpc-lesioned rats in the spatial version of the water maze. Lesion of the SNpc did not affect learning of the spatial version of the water maze. Pretraining non-lesioned rats in the cued version also improved their performance in the spatial version. These results suggest that hippocampal and nigrostriatal memory systems can work independently but can share information and mutually compensate learning if one system is damaged. This interpretation encourages cognitive training to compensate for memory deficits in Parkinson’s disease patients.