DL-AP5

Research use only, not for human use.

DL-AP5 is the racemic version of the selective N-methyl-D-aspartate (NMDA) receptor antagonist,with anticonvulsant.DL-AP5, a competitive NMDAR antagonist, on tramadol state-dependent memory. A single-trial step-down passive avoidance task was used for the assessment of memory retrieval in adult male NMRI mice.

DL-AP5 is the racemic version of the selective N-methyl-D-aspartate (NMDA) receptor antagonist,with anticonvulsant.DL-AP5, a competitive NMDAR antagonist, on tramadol state-dependent memory. A single-trial step-down passive avoidance task was used for the assessment of memory retrieval in adult male NMRI mice. Post-training i.p. administration of an atypical μ-opioid receptor agonist, tramadol (2.5 and 5 mg/kg), dose-dependently induced impairment of memory retention. Pre-test injection of tramadol (2.5 and 5 mg/kg) induced state-dependent retrieval of the memory acquired under post-training administration of tramadol (5 mg/kg) influence. Pre-test intra-CA1 injection of NMDA (10-5 and 10-4 μg/mouse) 5 min before the administration of tramadol (5 mg/kg, i.p.) dose-dependently inhibited tramadol state-dependent memory. Pre-test intra-CA1 injection of DL-AP5 (0.25 and 0.5 μg/mouse) reversed the memory impairment induced by post-training administration of tramadol (5 mg/kg). Pre-test administration of DL-AP5 (0.25 and 0.5 μg/mouse) with an ineffective dose of tramadol (1.25 mg/kg) restored the retrieval and induced tramadol state-dependent memory. It can be concluded that dorsal hippocampal NMDAR mechanisms play an important role in the modulation of tramadol state-dependent memory.

DL-AP5 (100 μM) partially prevents glutamate-induced increase in Arc/Arg3.1 protein levels.DL-AP5 decreases the NMDA-induced Arc/Arg3.1 upregulation.

DL-AP5 (0-10 μg/rat, Intra-CA1) significantly decreases the effect of NMDA.DL-AP5 (0-10 nmol, Intracerebroventricular injection) causes a dose-dependent increase in food consumption.DL-AP5 (5 nmol, Intracerebroventricular injection) attenuates the decreased food consumption induced by the intracerebroventricular injection of ghrelin. Animal Model:Male Wistar rats (180-230 g)Dosage:1, 3.2 and 10 μg/rat Administration:Injected into the intra-dorsal hippocampal (intra-CA1) immediately after shock administration, once Result:Significantly decreased the effect of NMDA (10-2 μg/rat, intra-CA1) with significant interaction.Animal Model:Broilers cockerels (3-h fooddeprived (FD3), n=8 for each group) Dosage:0, 2.5, 5, and 10 nmol; in a volume of 10 μL Administration:Intracerebroventricular injection Result:Caused a dose-dependent increase in food consumption which was significant for 5 and 10 nmol doses.Animal Model:Broilers cockerels (3-h fooddeprived (FD3), n=8 for each group) Dosage:5 nmol Administration:Intracerebroventricular injection, followed by ghrelin (0.6 nmol)Result:Attenuated the decreased food consumption induced by the intracerebroventricular injection of ghrelin.

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Membrane Transporter/Ion Channel

NMDAR

NMDA

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76326-31-3

197.13

C5H12NO5P

>98% (HPLC)

In Vitro:?H2O : 33.33 mg/mL (169.08 mM)

NC(CCCP(O)(O)=O)C(O)=O

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(-20℃)

With Ice Pack

≥ 2 years