D-2,4-Diaminobutyric acid dihydrochloride
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D-2,4-Diaminobutyric acid dihydrochloride

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Category
D-Amino Acids
Catalog number
BAT-007201
CAS number
26908-94-1
Molecular Formula
C4H10N2O2·2HCl
Molecular Weight
191.14
D-2,4-Diaminobutyric acid dihydrochloride
IUPAC Name
(2R)-2,4-diaminobutanoic acid
Synonyms
D-Dab-OH 2HCl; (R)-2,4-Diaminobutyric acid dihydrochloride; D Dab OH 2HCl
Purity
98%
Density
1.218
Storage
Store at 2-8 °C
InChI
InChI=1S/C4H10N2O2/c5-2-1-3(6)4(7)8/h3H,1-2,5-6H2,(H,7,8)/t3-/m1/s1
InChI Key
OGNSCSPNOLGXSM-GSVOUGTGSA-N
Canonical SMILES
C(CN)C(C(=O)O)N
1. Temperature dependence of N-methyl-D-aspartate receptor channels and N-methyl-D-aspartate receptor excitatory postsynaptic currents
M Korinek, M Sedlacek, O Cais, I Dittert, L Vyklicky Jr Neuroscience. 2010 Feb 3;165(3):736-48. doi: 10.1016/j.neuroscience.2009.10.058. Epub 2009 Oct 31.
N-methyl-d-aspartate (NMDA) receptors (NMDARs) are highly expressed in the CNS and mediate the slow component of excitatory transmission. The present study was aimed at characterizing the temperature dependence of the kinetic properties of native NMDARs, with special emphasis on the deactivation of synaptic NMDARs. We used patch-clamp recordings to study synaptic NMDARs at layer II/III pyramidal neurons of the rat cortex, recombinant GluN1/GluN2B receptors expressed in human embryonic kidney (HEK293) cells, and NMDARs in cultured hippocampal neurons. We found that time constants characterizing the deactivation of NMDAR-mediated excitatory postsynaptic currents (EPSCs) were similar to those of the deactivation of responses to a brief application of glutamate recorded under conditions of low NMDAR desensitization (whole-cell recording from cultured hippocampal neurons). In contrast, the deactivation of NMDAR-mediated responses exhibiting a high degree of desensitization (outside-out recording) was substantially faster than that of synaptic NMDA receptors. The time constants characterizing the deactivation of synaptic NMDARs and native NMDARs activated by exogenous glutamate application were only weakly temperature sensitive (Q(10)=1.7-2.2), in contrast to those of recombinant GluN1/GluN2B receptors, which are highly temperature sensitive (Q(10)=2.7-3.7). Ifenprodil reduced the amplitude of NMDAR-mediated EPSCs by approximately 50% but had no effect on the time course of deactivation. Analysis of GluN1/GluN2B responses indicated that the double exponential time course of deactivation reflects mainly agonist dissociation and receptor desensitization. We conclude that the temperature dependences of native and recombinant NMDAR are different; in addition, we contribute to a better understanding of the molecular mechanism that controls the time course of NMDAR-mediated EPSCs.
2. Mechanism and properties of positive allosteric modulation of N-methyl-d-aspartate receptors by 6-alkyl 2-naphthoic acid derivatives
Kiran Sapkota, et al. Neuropharmacology. 2017 Oct;125:64-79. doi: 10.1016/j.neuropharm.2017.07.007. Epub 2017 Jul 11.
The theory that N-methyl-d-aspartate receptor (NMDAR) hypofunction is responsible for the symptoms of schizophrenia is well supported by many pharmacological and genetic studies. Accordingly, positive allosteric modulators (PAMs) that augment NMDAR signaling may be useful for treating schizophrenia. Previously we have identified several NMDAR PAMs containing a carboxylic acid attached to naphthalene, phenanthrene, or coumarin ring systems. In this study, we describe several functional and mechanistic properties of UBP684, a 2-naphthoic acid derivative, which robustly potentiates agonist responses at each of the four GluN1a/GluN2 receptors and at neuronal NMDARs. UBP684 increases the maximal l-glutamate/glycine response while having minor subunit-specific effects on agonist potency. PAM binding is independent of agonist binding, and PAM activity is independent of membrane voltage, redox state, and the GluN1 exon 5 N-terminal insert. UBP684 activity is, however, markedly pH-dependent, with greater potentiation occurring at lower pHs and inhibitory activity at pH 8.4. UBP684 increases channel open probability (Po) and slows receptor deactivation time upon removal of l-glutamate, but not glycine. The structurally related PAM, UBP753, reproduced most of these findings, but did not prolong agonist removal deactivation time. Studies using cysteine mutants to lock the GluN1 and GluN2 ligand-binding domains (LBDs) in the agonist-bound states indicate that PAM potentiation requires GluN2 LBD conformational flexibility. Together, these findings suggest that UBP684 and UBP753 stabilize the GluN2 LBD in an active conformation and thereby increase Po. Thus, UBP684 and UBP753 may serve as lead compounds for developing agents to enhance NMDAR activity in disorders associated with NMDAR hypofunction.
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