Comparison of bilaterally 6-OHDA- and MPTP-lesioned rats as models of the early phase of Parkinson's disease: histological, neurochemical, motor and memory alterations.

This study compares histological, neurochemical, behavioral, motor and cognitive alterations as well as mortality of two models of Parkinson's disease in which 100 microg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 6 microg 6-hydroxydopamine (6-OHDA) was bilaterally infused into the central region of the substantia nigra, compact part, of adult male Wistar rats. Both neurotoxins caused a significant loss of nigral tyrosine hydroxylase-immunostained cells and striatal dopamine depletion, but 6-OHDA caused more widespread and intense cell loss, more intense body weight loss and more mortality than MPTP. Both 6-OHDA- and MPTP-lesioned rats presented similar deficits in performing a working memory and a cued version of the Morris water maze task and few exploratory/motor alterations in the open field and catalepsy tests.

Is the unilateral lesion of the left substantia nigra pars compacta sufficient to induce working memory impairment in rats?

Adult male Wistar rats with a substantia nigra pars compacta (SNc) lesion induced by intranigral administration of 1 micromol 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were used as a model of early phase Parkinson's disease (PD). This lesion caused a partial depletion of striatal dopamine (DA). The animals were submitted to a spatial working memory version of the water maze task in which they had to find a hidden (submersed) platform using online-maintained information that the platform remains in the same place during four consecutive trials, but that it is moved to another place every training day.

Amino acid and monoamine alterations in the cerebral cortex and hippocampus of mice submitted to ricinine-induced seizures.

The alkaloid ricinine isolated from the plant Ricinus communis, when administered to mice at high doses, induces clonic seizures accompanied by electroencephalographic alterations in the cerebral cortex and hippocampus. The lethal nature of ricinine-induced seizures is considered to be a good model for the study of the events that cause death during clonic seizures, particularly those related to respiratory spasms. The initial signs (pre-seizure period) were marked by exophthalmus and decreased locomotor behavior.