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125229-62-1

125229-62-1 Structure

125229-62-1 Structure
IdentificationBack Directory
[Name]

AP-5 LITHIUM SALT
[CAS]

125229-62-1
[Synonyms]

AP-5 LITHIUM SALT
DL-2-AMINO-5-PHOSPHONOVALERIC ACIDLITHIU M
DL-2-Amino-5-phosphonopentanoic acid, AP-5
DL-2-AMINO-5-PHOSPHONOVALERIC ACID LITHIUM SALT
DL-2-AMINO-5-PHOSPHONOPENTANOIC ACID LITHIUM SALT
DL-2-AMino-5-phosphonovaleric acid lithiuM salt ~95%
[Molecular Formula]

C5H11LiNO5P
[MDL Number]

MFCD00078901
[MOL File]

125229-62-1.mol
[Molecular Weight]

203.06
Chemical PropertiesBack Directory
[form ]

powder
[color ]

white to off-white
Safety DataBack Directory
[WGK Germany ]

3
Hazard InformationBack Directory
[Uses]

DL-AP5 (2-APV) lithium is a competitive NMDA (N-methyl-D-aspartate) receptor antagonist. DL-AP5 lithium shows significantly antinociceptive activity. DL-AP5 lithium specifically blocks on channels in the rabbit retina[1][2][3].
[Biological Activity]

DL-2-Amino-5-phosphonovaleric acid is a selective N-methyl-d-aspartate (NMDA) receptor antagonist used frequently in studies of neurological processes''Anticonvulsant; potent and selective antagonist for NMDA receptors.
[in vivo]

DL-AP5 (0-10 μg/rat, Intra-CA1) significantly decreases the effect of NMDA[3].
DL-AP5 (0-10 nmol, Intracerebroventricular injection) causes a dose-dependent increase in food consumption[4].
DL-AP5 (5 nmol, Intracerebroventricular injection) attenuates the decreased food consumption induced by the intracerebroventricular injection of ghrelin[4].

Animal Model:Male Wistar rats (180-230 g)[3]
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)[4]
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)[4]
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.
[IC 50]

NMDA Receptor
[References]

[1] Murray CW, et al. Neurokinin and NMDA antagonists (but not a kainic acid antagonist) are antinociceptive in the mouse formalin model. Pain. 1991;44(2):179-185. DOI:10.1016/0304-3959(91)90135-K
[2] Massey SC, et al. N-methyl-D-aspartate receptors of ganglion cells in rabbit retina. J Neurophysiol. 1990;63(1):16-30. DOI:10.1152/jn.1990.63.1.16
[3] Jafari-Sabet M. NMDA receptor blockers prevents the facilitatory effects of post-training intra-dorsal hippocampal NMDA and physostigmine on memory retention of passive avoidance learning in rats. Behav Brain Res. 2006 Apr 25;169(1):120-7. DOI:10.1016/j.bbr.2005.12.011
[4] Taati M, et al. The effects of DL-AP5 and glutamate on ghrelin-induced feeding behavior in 3-h food-deprived broiler cockerels. J Physiol Biochem. 2011 Jun;67(2):217-23. DOI:10.1007/s13105-010-0066-y
[5] Chen T, et al. Glutamate-induced rapid induction of Arc/Arg3.1 requires NMDA receptor-mediated phosphorylation of ERK and CREB. Neurosci Lett. 2017 Nov 20;661:23-28. DOI:10.1016/j.neulet.2017.09.024
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