Résumé
To explore the role and changes of dopamine receptor activity and their subtypes during the onset process of Parkinson disease( PD ), on the basis of 6 hydroxydopamine lesioned PD rat model, radioligand binding assay (RLBA) and Scanchard drawing were used to measure the maximal binding capacity of receptor (Bmax) and equilibrium dissociation constant (KD) of D 1 and D 2 dopamine receptors in caudal putamen of the model and control rats at different time point. The results of RLBA study revealed D 2 dopamine receptor Bmax was significantly increased and KD was significantly decreased in the caudal putamen ipsilateral to the lesion in rat model, and the changes reached the peak in one month rat model group. In contrast, the caudal putamen D 1 receptors were far less affected, with no consistent changes in the same model groups as compared with the control, except that 2 weeks model group showed Bmax was slightly decreased while KD was slightly increased. The study confirms that D 2 dopamine receptor is upregulated in the caudal putamen ipsilateral to the lesion in PD rat model, and the affinity of the receptors is increased, but the activity of D 1 dopamine receptor is not significantly changed.
Résumé
AIM: To investigate the effects of glioma cells on aquaporin expression in blood-brain barrier and their importance in pathophysiology. METHODS: A blood-brain barrier model was established by coculture of ECV304 and astrocytes in vitro . HPLC was used to determine the change of water transport of in vitro blood-brain barrier model after the influence of glioma cells. The expression levels of AQP1 and AQP4 were analyzed by semiquatitative RT-PCR. RESULTS: Glioma cells decreased expression level of AQP4 of astrocytes and induced abnormal expression of aquaporin-1 in endothelial cell line. The water transport of in vitro blood-brain barrier model from luminal side to abluminal side was increased after coculture with glioma cells. CONCLUSION: The vasogenic brain edema induced by glioma cells may not be the result of hyperpermeability of blood-brain barrier to macromolecules in plasma. The changes of aquaporin expression may be the molecular basis of brain edema induced by glioma cells.