Both lesion types caused impaired response accuracy, which was more pronounced when responses had to be directed contralateral to the lesion. Furthermore, movement times were increased for both lesion learn more groups, whereas only the bundle

lesion group displayed a RT deficit. The lesions were stable over three consecutive weeks of testing, therefore lesion-type and behavioural assessment on the operant task are suitable to investigate the dopaminergic system in parkinsonian mice. Both lesions were stable over time, and were more pronounced when responses were directed in contralateral space; the mice with more complete bundle lesions displayed a greater deficit than mice that received lesions to the SN. The translation of this choice RT task will be beneficial for the assessment of therapeutics in mouse models of the disease. “
“Several

studies have revealed that manipulation of the renin angiotensin system results in reduced progression of nigrostriatal damage in different animal models of Parkinson’s disease. In the present work, the effect of daily treatment of rats with the angiotensin II (Ang II) type 1 (AT1) receptor antagonist candesartan (3 mg/kg per day, s.c.) initiated 7 days before the intrastriatal injection of 6-hydroxydopamine (6-OHDA) was investigated by means of tyrosine hydroxylase-positive cell counts in the substantia nigra, and IDO inhibitor dopamine and 3,4-dihydroxyphenylacetic acid measurements in the striatum. In this experimental set-up, candesartan protected dopaminergic neurons of the nigrostriatal tract against the neurotoxin-induced cell death. However, the beneficial effects of AT1 receptor blockade were not confirmed when treatment was started 24 h after the lesion, suggesting that candesartan see more interferes with the early events of the 6-OHDA-induced cell death. Stimulation of the AT1 receptor with Ang II increased the formation of hydroxyl

radicals in the striatum of intact rats as measured by the in vivo microdialysis salicylate trapping technique. This Ang II-induced production of reactive oxygen species was suppressed by candesartan perfusion. Furthermore, the Ang II-induced production of reactive oxygen species was nicotinamide adenine dinucleotide phosphate – oxidase and protein kinase C dependent as it could be blocked in the presence of apocynin, an nicotinamide adenine dinucleotide phosphate – oxidase inhibitor, and chelerythrine, an inhibitor of protein kinase C. Together, these data further support the hypothesis that Ang II might contribute in an early stage to the neurotoxicity of 6-OHDA by reinforcing the cascade of oxidative stress. “
“In both monkeys and humans, reaching-related sensorimotor transformations involve the activation of a wide fronto-parietal network. Recent neurophysiological evidence suggests that some components of this network host not only neurons encoding the direction of arm reaching movements, but also neurons whose involvement is modulated by the intrinsic features of an object (e.g.