To induce parkinsonism, You have to destroy striatal dopaminergic tracts.Hence you have administer it strereotactically in to the brain, using a rat stereotaxic frame.
To induce parkinsonism, You have to destroy striatal dopaminergic tracts.Hence you have administer it strereotactically in to the brain, using a rat stereotaxic frame.
But i've came across a paper in which they've induced pd by iv infusion in monkey
No doubt, people have used peripheral means to infuse 6-OHDA to induce Parkinsonism. But this route will not produce a proper lesion in the nigro-striatal tract because of the poor BBB crossing of 6-OHDA.
For a comprehensive review on this matter please refer to the following review.
Jordi Bové, Delphine Prou, Céline Perier, and Serge Przedborski. Toxin-induced models of Parkinson’s Disease. NeuroRx. 2005 July; 2(3): 484–494
Our PD-models are in this and related paper:
Fredriksson, Anders; Stigsdotter, Ingels Maria; Hurtig, Anders; Ewalds-Kvist, Béatrice; Archer, Trevor. Running wheel activity restores MPTP-induced functional deficits.
Journal of Neural Transmission118.3 (Mar 2011): 407-420.
6-hydroxydopamine–lesioned mice are used in:
Bonito-Oliva, Alessandra; Pignatelli, Marco; Spigolon, Giada; Yoshitake, Takashi; Seiler, Stefanie; et al. (2014). Cognitive impairment and dentate gyrus synaptic dysfunction in experimental parkinsonism.
Biological Psychiatry75.9 (May 1, 2014): 701-710.
Methods: We studied cognitive performance and synaptic plasticity in a mouse model of PD, characterized by partial lesion of the dopaminergic and noradrenergic inputs to striatum and hippocampus. Sham– and 6-hydroxydopamine–lesioned mice were subjected to the novel object recognition test, and long-term potentiation was examined in the dentate gyrus and CA1 regions of the hippocampus. Results: Bilateral 6-hydroxydopamine lesion reduced long-term but not short-term novel object recognition and decreased long-term potentiation specifically in the dentate gyrus. These abnormalities did not depend on the loss of noradrenaline but were abolished by the antiparkinsonian drug, L-DOPA, or by SKF81297, a dopamine D1-type receptor agonist. In contrast, activation of dopamine D2-type receptors did not modify the effects produced by the lesion. Blockade of the extracellular signal-regulated kinases prevented the ability of SKF81297 to rescue novel object recognition and long-term potentiation. Conclusions: These findings show that partial dopamine depletion leads to impairment of long-term recognition memory accompanied by abnormal synaptic plasticity in the dentate gyrus. They also demonstrate that activation of dopamine D1 receptors corrects these deficits, through a mechanism that requires intact extracellular signal-regulated kinases signaling.
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