Selective destruction of nigrostriatal dopaminergic neurons does not alter [3H]-ryanodine binding in rat striatum

Dopamine nigrostriatal neurons are important for motor control and may contain a particularly dense population of ryanodine receptors involved in the control of dopamine release. To test this hypothesis, we used a classical model of unilateral selective lesion of these neurons in rats based on 6-hydroxydopamine (6-OHDA) injection into the substantia nigra. Binding of [3H]-GBR 12935, used as a presynaptic marker since it labels specifically the dopamine uptake complex, was dramatically decreased by 83-100 percent in striatum homogenates after 6-OHDA lesion. On the contrary, no reduction of [3H]-ryanodine binding was observed. The present data indicate that [3H]-ryanodine binding sites present in rat striatum are not preferentially localized in dopaminergic terminals

cytological effects of a neurotrophic peptide [MPF] in Parkinsonian rats

Substantia nigra [SN] samples from rats with 6-hydroxdopamine [6-OHDA] -induced lesions of right nigrostriatal pathways were retrieved and examined by transmission electron microscopy [TEM] 15-17 months after a single intrastriatal injection of a metabolically-stable analogue of Lys-Lys-Gly-Glu [MPF] in Krebs-Hensleitt buffer, given two weeks after the lesioning. The results were compared with those from control samples taken from rats which had been similarly lesioned and kept for 15-17 months, but which had received only Krebs-Hensleitt buffer, and with samples taken from two age matched, non-lesioned rats. Compared with the age matched, non-lesioned rats, there was a 37% overall loss of and extensive damage to all surviving SN neurons in samples from control rats [lesioned, buffer only]. There was widespread collapse of mitochondria [63% in the case of dopaminergic neurons], loss of cell membranes [in 4.4% of cases], myelin abnormalities [9.0%] and increased vacuolation [10.9%]. In contrast, most of the SN neurons from MPF-treated rats were healthy reflected in a high degree of cellular organization and integration; only 9.0% of the mitochondria were collapsed, and the cell membranes damage [2.9%] myelin abnormalities [1.5%], and the increased vacuolation [2.6%] were significantly less than found in the control rats. We have previously reported a significant reduction in the amphetamine-induced turning behaviour of lesioned rats following injection of the MPF analogue, beginning 6 weeks after the MPF injection, and reaching marked and consistent levels after 12 weeks. This time course, in conjunction with the present results and known neurotrophic properties of MPF, suggest that the favourable behavioural effects of MPF arise by restoration of nigrostriatal pathways

Modelo animal del disturbio de hiperactividad con déficit de atención / Animal model of attention deficit disorder with hyperactivity

Los autores estudiaron un modelo animal de disturbio de hiperactividad con déficit de atención (DHDA), siendo estudiados 25 ratones Wistar recién nacidos de ambos sexos, divididos en 3 grupos I control, con 8 animales; grupo II 6-OHDA, con 9 animales y el grupo III DMI + 6 - OHDA, con 8 animales. Los animales fueron observados en el campo abierto a los 21 días, a los 30 días y a los 53 días, en la esquiva pasiva a los 35 días de vida. Los resultados mostraron que ratones jóvenes con lesión dopaminérgica o lesión dopaminérgica y noradrenérgica tuvieron aumento significativo del parámetro andar, a los 21 y a los 30 días. La lesion dopaminérgica fue la más importante en la génesis de la hiperactividad. En la esquiva pasiva no hubo diferencias entre los animales lesionados y los controles