Disease relevance of 5-Phosphononorvaline

• The LTP induced by 100 Hz tetanus was blocked by 50-100 microM DL-2-amino-5-phosphonovaleric acid, suggesting that N-methyl-D-aspartate receptors were responsible for its induction [1].
• At a concentration of 250 microM, 2-amino-5-phosphonovalerate (APV) blocked the responses of all ganglion cells to NMA, but not to QA or KA, indicating that NMA acts at different receptor sites from QA or KA [2].
• Furthermore, thermal hyperalgesia was significantly inhibited by the N-methyl-D-aspartate (NMDA) receptor antagonists, 2-amino-5-phosphonopentanoate (APV), dizocilpine and ifenprodil [3].
• Metaphit, a proposed PCP-receptor acylator, and 2-amino-5-phosphonovalerate (AP5), an N-methyl-D-aspartate (NMDA) antagonist, produced complete PCP-appropriate responding in the high training dose group only at doses that suppressed the rate of responding and that produced ataxia [4].
• Actions of D and L forms of 2-amino-5-phosphonovalerate and 2-amino-4-phosphonobutyrate in the cat spinal cord [5].

Psychiatry related information on 5-Phosphononorvaline

• Evidence for functional differences between entopeduncular nucleus and substantia nigra: effects of APV (DL-2-amino-5-phosphonovaleric acid) microinfusion on reaction time performance in the rat [6].
• Intra-accumbens infusion of the competitive NMDA receptor antagonist, DL-2-amino-5-phosphonovaleric acid (AP-5) (2, 4 and 10 micrograms/0.5 microliters) induced a dose-dependent increase in locomotor activity in rats [7].

High impact information on 5-Phosphononorvaline

• The effect was completely absent at 32 degrees C and was blocked by both the N-methyl-D-aspartate receptor antagonist, 2-amino-5-phosphonovalerate and the inhibitor of nitric-oxide synthase, L-nitro-arginine methyl ester [8].
• Excitatory synaptic inputs were blocked by the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) and by the NMDA receptor antagonist 2-amino-5-phosphonopentanoate (AP-5; 50 microM) [9].
• This potentiation of the EPSP by 17 beta-estradiol still occurred in the presence of the NMDA antagonist 2-amino-5-phosphonovalerate, but was blocked by the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione [10].
• The monosynaptically evoked IPSC in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and dl-2-amino-5-phosphonovaleric acid (APN) was also diminished following a train of action potentials; however, iontophoretically applied GABA responses did not change significantly [11].
• Exposure to 100 microM DL-2-amino-5-phosphonovaleric acid (APV), an antagonist of the NMDA channel, during the stimulation period prevented the competitive advantage associated with electric stimulation [12].

Chemical compound and disease context of 5-Phosphononorvaline

• Finally, habituation of gill withdrawal requires activation of NMDA-type and AMPA-type postsynaptic receptors within the abdominal ganglion, because it is blocked by infusion of dl-2-amino-5-phosphonovaleric acid or 6,7-dinitroquinoxaline-2,3-dione [13].

Biological context of 5-Phosphononorvaline

• Phosphorylation of GluRs in response to Glu/Gly was blocked by a specific NMDA receptor/ion channel antagonist (DL-2-amino-5-phosphonovaleric acid) or by a cell-permeable inhibitor of CaM-kinase II (1-[N,O-bis(1,5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4- phenylpiperazine, KN-62) [14].
• NMDA antagonists [MK-801 and 2-amino-5-phosphonovalerate (APV)] induced cell shrinkage, nuclear condensation or fragmentation, and internucleosomal DNA fragmentation [15].
• The NMDA receptor antagonists MK-801 and 2-amino-5-phosphopentanoic acid markedly prevented the age-induced apoptosis of CGCs, and the cells survived >18 DIV under these conditions [16].
• N-methyl-D-aspartate receptor channels are necessary for induction of this depolarization, as well as for long-term potentiation, as demonstrated by the effect of DL-2-amino-5-phosphonovaleric acid [17].
• Whereas the monosynaptic reflex was relatively resistant to N-methyl-D-aspartate antagonists [Mg++, 2-amino-5-phosphonovalerate (APV) and 2-amino-7-phosphonoheptanoate (AP7)], the polysynaptic reflex was markedly reduced in a concentration-dependent manner [18].

Anatomical context of 5-Phosphononorvaline

• Earlier studies found that chronic treatment of the optic tectum with the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (DL-AP5) desegregated eye-specific stripes in three-eyed frogs, while chronic treatment with NMDA sharpened stripe borders (Cline et al., 1987; Cline and Constantine-Paton, 1990) [19].
• The present experiment tested the hypothesis that the attentional impairments produced by bilateral basal forebrain infusions of the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV) are associated with attenuation of performance-associated increases in ACh release [20].
• We studied identified rat retinal ganglion cell neurons in vitro, a useful system for the study of excitotoxicity, and compared the protective effects of delayed administration of a competitive antagonist, 2-amino-5-phosphonovalerate (APV), and of an uncompetitive antagonist, MK-801, after glutamate-induced injury [21].
• Recordings were obtained from somata and apical dendrites in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), DL-2-amino-5-phosphonovaleric acid (APV), and bicuculline [22].
• One week later, 2-amino-5-phosphono-pentanoic acid (AP-5; 10 micrograms/rat), a specific competitive NMDA receptor antagonist; 6,7-dinitroquinoxaline-2,3-dione (DNQX; 30 nM), a selective antagonist of non-NMDA receptors; or the same volume of saline, was injected via the third ventricle to conscious and unrestrained ovariectomized animals [23].

Associations of 5-Phosphononorvaline with other chemical compounds

• In contrast, intra-VTA infusion of the NMDA receptor antagonist 2-amino-5-phosphopentanoic acid (100 and 500 microM) dose-dependently decreased the striatal release of dopamine [24].
• This increase was both NMDA- and glycine-dependent and was inhibited by competitive and noncompetitive NMDA antagonists, including 2-amino-5-phosphopentanoic acid and MK-801 [25].
• The effect of suramin was completely abolished by adenylimidodiphosphate, a non-hydrolyzable analogue of ATP, and markedly reduced by NMDA-receptor antagonists DL-2-amino-5-phosphonovaleric acid and MK-801 [26].
• The N-methyl-D-aspartate receptor-selective antagonist 2-amino-5-phosphonopentanoate (100 microM) blocked the effect of N-methyl-D-aspartate but not the effects of AMPA, kainate and glutamate [27].
• Ethanol did not occlude the effects of a low concentration of 2-amino-5-phosphonovalerate, an antagonist with less N-methyl-d-aspartate receptor subtype selectivity [28].

Gene context of 5-Phosphononorvaline

• The selective antagonists 2-amino-5-phosphonovalerate (100 microM) and MK-801 (1 microM) blocked the N-methyl-D-aspartate-evoked release of somatostatin-like immunoreactivity; KCl-evoked release was unaffected [29].
• On this basis, to verify the above hypothesis, we determined the release level of IL-1beta and IFN-gamma cytokines in media of cultured rat hippocampal neurons under physiological and anoxic conditions with and without 2-amino-5-phosphonopentanoate (AP5; an N-methyl-D-aspartate receptor antagonist) [30].
• In addition, responses to NAAG were completely antagonized by 250 microM DL-2-amino-5-phosphonovaleric acid, a specific NMDA-receptor antagonist [31].
• The N-methyl-D-aspartate receptor antagonist, DL-2-amino-5-phosphonovaleric acid (50 microM), inhibited induction of long-term potentiation, redistribution of protein kinase C and phosphorylation of growth-associated protein 43 [32].
• In the third experiment, an intraventricular dose (20 micrograms) of an N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonovalerate (APV) was used to block the basal-dendritic LTP in CA1 [33].

Analytical, diagnostic and therapeutic context of 5-Phosphononorvaline

• In the immature slices, bathed in normal (Mg2+-containing) medium, 2-amino-5-phosphonovalerate caused a small reduction in the short latency potential and inhibited a component of the slow negative wave which could, again, be observed in relative isolation after perfusion of 6-cyano-2,3-dihydroxy-7-nitro-quinoxaline [34].
• This sympathoexcitatory response was eliminated by prior microinjection of DL-2-amino-5-phosphonovaleric acid, an antagonist of the NMDA receptor [35].
• At these concentrations, intrathecal administration of 2-amino-5-phosphonovalerate to awake mice produced significant analgesia on a battery of tests, as well as a dose-related motor impairment, while glutamylaminomethylsulphonate was without effect [36].
• Experiments were performed with the patch pipette containing either a low-calcium internal saline to allow comparison with subsequent whole cell recordings or external saline with tetrodotoxin, DL-2-amino-5-phosphonovaleric acid, and 6-cyano-7-nitroquinoxaline-2,3-dione, a solution that is more appropriate for bathing a nerve terminal [37].
• The PIP was not affected by 2-amino-5-phosphonovalerate (APV) administered via microdialysis at 7 h post-ischemia [38].

References