D-AP5 is a NMDA receptor antagonist. Chronic intraventricular infusion of D-AP5 causes a parallel dose-dependent impairment of spatial learning and long-term potentiation (LTP) in vivo. Intracerebral concentrations of D-AP5 fail to induce any measurable sensorimotor disturbance when spatial learning is prevented[1]. D-AP5 infusion is associated with a progressive reduction in swim speed over trials. D-AP5 causes sensorimotor disturbances in the spatial task, but these gradually worsened as the animals fail to learn. Rats treated with D-AP5 show a delay-dependent deficit in spatial memory in the delayed matching-to-place protocol for the water maze[2].
In Vitro
Kinase Assay
Cell Assay
Animal Administration
Male Lister hooded rats are used in this study. They are housed individually and have free access to food and water at all times except for 12 hr prior to surgery. Animals are implanted with 30 mM D-AP5 (N=6) and tested in the water maze[1].
References
[1]. Davis S, et al. The NMDA receptor antagonist D-2-amino-5-phosphonopentanoate (D-AP5) impairs spatial learning and LTP in vivo at intracerebral concentrations comparable to those that block LTP in vitro. J Neurosci. 1992 Jan;12(1):21-34.
[2]. Morris RG, et al. N-methyl-d-aspartate receptors, learning and memory: chronic intraventricular infusion of the NMDA receptor antagonist d-AP5 interacts directly with the neural mechanisms of spatial learning. Eur J Neurosci. 2013 Mar;37(5):700-17.
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