作者: A. Pintor , M.T. Tebano , A. Martire , R. Grieco , M. Galluzzo
DOI: 10.1016/J.NEUROPHARM.2006.06.013
关键词:
摘要: The ability of CB(1) receptors to regulate the release glutamate in striatum, together with finding that, experimental models Huntington disease (HD), both endocannabinoid levels and receptor densities are reduced, has prompted investigation on neuroprotective role cannabinoids HD. Quinolinic acid (QA) is an excitotoxin when injected rat striatum reproduces many features HD that acts by stimulating outflow. aim present study was test cannabinoid agonist WIN 55,212-2 prevent effects induced QA striatum. In microdialysis experiments, probe perfusion significantly dose-dependently prevented increase extracellular QA. electrophysiological recordings corticostriatal slices, application QA-induced reduction field potential amplitude. Both were antagonist AM 251. vivo intrastriatal attenuated striatal damage QA, although no significant observed a behavioural ground. These data demonstrate stimulation might lead against excitotoxic toxicity.