Disease relevance of DL-2-Amino-7-phosphonoheptanoic acid

• Focal microinfusion into the dorsal hippocampus of 2-amino-7-phosphonoheptanoic acid, an antagonist of excitation at the N-methyl-D-aspartate-preferring receptor, before ischemia was induced protected against the development of ischemic damage [1].
• Pretreatment of rats with the excitatory amino acid antagonist 2-amino-7-phosphonoheptanoic acid (2-APH; 0.5 mmol/kg, i.p.) protected against insulin-induced clonic seizures [2].
• 2-Amino-7-phosphonoheptanoic acid raises the onset pressure for all three phases of HPNS in fed rats, but only for tremor and convulsions in fasted rats [3].
• The intraperitoneal administration of the competitive NMDA receptor blocker DL-2-amino-7-phosphonoheptanoic acid (36 and 72 mg/kg) and the non-competitive NMDA receptor blocker MK-801 (1.35 and 2.7 mg/kg), completely prevented the induction of seizure and bradyarrhythmia or sudden death resulting from seizure [4].
• Enhancement of lordosis/mounts quotient (L/M) by progesterone (0.5 mg) or LH-RH (150 ng; third ventricle, IVT) in OVX-EB rats was significantly decreased by IVT injection of (+) 2-amino-7-phosphonoheptanoic acid a competitive N-methyl-D-aspartic acid (NMDA) receptor antagonist [5].

Psychiatry related information on DL-2-Amino-7-phosphonoheptanoic acid

• Haloperidol pretreatment prevents stereotyped behaviour induced by 2-amino-7-phosphonoheptanoic acid, but does not change the effect on the electroshock test [6].

High impact information on DL-2-Amino-7-phosphonoheptanoic acid

• Local injections of an NMDA receptor antagonist, 2-amino-7-phosphonoheptanoic acid, were performed before induction of 30 minutes of reversible, insulin-induced, hypoglycemic coma [7].
• Kainic acid (KA) produced an upregulation of hippocampal and neocortical BDNF mRNA as well as BDNF protein that was blocked by a non-NMDA antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), but was not affected by the NMDA antagonist 2-amino-7-phosphonoheptanoic acid (AP7) [8].
• Biphenyl-derivatives of 2-amino-7-phosphonoheptanoic acid, a novel class of potent competitive N-methyl-D-aspartate receptor antagonist--I. Pharmacological characterization in vitro [9].
• Infusions of 2-amino-7-phosphonoheptanoic acid (AP7) or ketamine into the substantia nigra pars reticulata (SNPR) of adult rats increase the latency of onset to seizures induced by the convulsant ether flurothyl [10].
• 2. Competitive (carboxypiperazine-propylphosphonic acid, CPP; 2-amino-7-phosphonoheptanoic acid, AP7) and non-competitive (MK801; phencyclidine, PCP; thienylcyclohexylpiperidine, TCP; dextrorphan; dextromethorphan) NMDA antagonists prevented NMDA-induced convulsions [11].

Chemical compound and disease context of DL-2-Amino-7-phosphonoheptanoic acid

• These and earlier data with 2-amino-7-phosphonoheptanoic acid suggest that excitation at the N-methyl-D-aspartate receptor is important in HPNS tremor, and that excitation at the quisqualate receptor contributes to HPNS convulsions [12].

Biological context of DL-2-Amino-7-phosphonoheptanoic acid

• 3. 2-Amino-7-phosphonoheptanoic acid blocked the ovulatory luteinizing hormone surge in proestrus rats [13].
• The elevated atmospheric pressure at which the main features of the high pressure neurological syndrome (HPNS), i.e. tremor, myoclonus and convulsions, successively appear, have been studied in fed and fasted rats with and without pretreatment with 2-amino-7-phosphonoheptanoic acid (180 mg/kg) [3].

Anatomical context of DL-2-Amino-7-phosphonoheptanoic acid

• Inhibition of high-affinity [3H]L-proline binding to rat brain membranes by 2-amino-7-phosphonoheptanoic acid [14].
• 2-Amino-7-phosphonoheptanoic acid depresses gamma-motoneurons and polysynaptic reflexes in the cat spinal cord [15].
• Suppression of amygdaloid kindled convulsion following unilateral injection of 2-amino-7-phosphonoheptanoic acid (2-APH) into the substantia innominata of rats [16].
• 2-Amino-7-phosphonoheptanoic acid (2-APH) infusion into entopeduncular nucleus protects against limbic seizures in rats [17].
• The study examined effects of a competitive NMDA receptor antagonist [dl-2-amino-7-phosphonoheptanoic acid (AP7)] or an alpha1 noradrenergic agonist (phenylephrine) focally microinjected into DLSC as compared to effects in the inferior colliculus (IC) and pontine reticular formation (PRF), which are major established components of the AGS network [18].

Associations of DL-2-Amino-7-phosphonoheptanoic acid with other chemical compounds

• The effects of nine clinically active antiepileptic drugs and the NMDA antagonist 2-amino-7-phosphonoheptanoic acid (2-APH) were examined in three models in the in vitro hippocampal slice [19].
• Biphenyl-derivatives of 2-amino-7-phosphono-heptanoic acid, a novel class of potent competitive N-methyl-D-aspartate receptor antagonists--II. Pharmacological characterization in vivo [20].
• The NMDA-receptor blockers, 2-amino-5-phosphonovaleric acid (APV) and 2-amino-7-phosphonoheptanoic acid (AP7), selectively and reversibly inhibited the glutamate-evoked oesophageal responses, but had no corresponding effect on rhythmic oesophageal responses elicited by muscarine [21].
• Intrahippocampal co- and post-administration of ibotenate with (-) 2-amino-7-phosphonoheptanoic acid entirely prevented or stopped the occurrence of both EEG changes and neuronal degeneration [22].
• Unilateral equimolar microinjections of 2-amino-7-phosphonoheptanoic acid (AP-7), an NMDA receptor antagonist, or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), a non-NMDA receptor antagonist, into AT were given prior to kainate administration [23].

Gene context of DL-2-Amino-7-phosphonoheptanoic acid

• In contrast, focal pretreatment of MD with a competitive antagonist of the NMDA receptor 2-amino-7-phosphonoheptanoic acid (500 pmol) did not attenuate seizures [24].
• The effects of the chronic intracerebroventricular (i.c.v.) infusion of the potent dicarboxylic amino acid antagonist, 2-amino-7-phosphonoheptanoic acid (APH), were examined in female rats as a prelude to the use of this compound in exploring the role of dicarboxylic amino acids in barbiturate dependence and withdrawal [25].
• Impaired motor coordination in mice induced by 2-amino-7-phosphonoheptanoic acid (APH), glutamic acid diethyl ester (GDEE), and other compounds [26].

Analytical, diagnostic and therapeutic context of DL-2-Amino-7-phosphonoheptanoic acid

• Microinjection of a competitive NMDA receptor antagonist, DL-2-amino-7-phosphonoheptanoic acid (AP7) (2 and 5 but not 1 nmol/side), into the PAG suppressed AGS, in part, reversibly [27].
• Cortical intraventricular injection of D-2-amino-5-phosphonovalerate (APV) and DL-2-amino-7-phosphonoheptanoic acid (APH) prevented induction of the potentiation in SII [28].
• The method was validated by measuring seizures generated by intraperitoneal injection of pentylenetetrazol (PTZ), by microinjection of excitatory amino acids into the dorsal hippocampus, and by the antagonism of these seizures by diazepam and 2-amino-7-phosphono heptanoic acid, respectively [29].

References