Synthesis of N-Boc-(R)-α-phenyl-γ-aminobutyric acid using an in situ diastereoselective protonation strategy

2002 ◽  
Vol 13 (3) ◽  
pp. 293-296 ◽  
Author(s):  
Monique Calmès ◽  
Françoise Escale ◽  
Jean Martinez
Keyword(s):  
1985 ◽  
Vol 249 (3) ◽  
pp. R372-R374 ◽  
Author(s):  
P. L. Lutz ◽  
R. Edwards ◽  
P. M. McMahon

Changes in gamma-aminobutyric acid (GABA) concentrations in the turtle (Pseudemys scripta elegans) brain were studied in situ during prolonged anoxia. With the onset of anoxia, the well-documented rapid increases in GABA found in mammalian brains were not observed in the turtle brain. Although not statistically significant, mean GABA concentrations in the turtle brain were reduced from anesthetized control values during the first 30 min of anoxia. During this initial period brain glutamate content declined. Even after 2 h of nitrogen respiration, GABA in the turtle brain still did not rise above control levels. By the 4th h of anoxia, however, GABA had increased to 147% of control values.


2011 ◽  
Vol 129 (2) ◽  
pp. 395-401 ◽  
Author(s):  
Iris J. Joye ◽  
Lieve Lamberts ◽  
Kristof Brijs ◽  
Jan A. Delcour

2004 ◽  
Vol 59 (8) ◽  
pp. 930-933 ◽  
Author(s):  
Bassam A. Abu Thaher ◽  
Jalal A. Zahra ◽  
Mustafa M. El-Abadelah ◽  
W. Voelter

Abstractγ -Aminobutyric acid (GABA) adds onto nitrile imine 1,3-dipolar species (generated in situ from their N-arylhydrazonoyl chloride precursors 1a-c ) to deliver the corresponding acyclic amidrazone adducts 10a-c. In the presence of 1,1’-carbonyldiimidazole, the latter adducts undergo cyclocondensation involving the activated carboxyl and the amidrazone-CH2NH groups to afford the respective N-[1-(arylhydrazono)-2-oxopropan-1-yl] pyrrolidin-2-ones (11a-c). The constitution of 10 and 11 is evidenced from analytical and spectral (IR , MS and NMR) data.


2019 ◽  
Vol 30 (3) ◽  
pp. 1393-1406
Author(s):  
N Forte ◽  
F Binda ◽  
A Contestabile ◽  
F Benfenati ◽  
P Baldelli

Abstract Neurotransmitters can be released either synchronously or asynchronously with respect to action potential timing. Synapsins (Syns) are a family of synaptic vesicle (SV) phosphoproteins that assist gamma-aminobutyric acid (GABA) release and allow a physiological excitation/inhibition balance. Consistently, deletion of either or both Syn1 and Syn2 genes is epileptogenic. In this work, we have characterized the effect of SynI knockout (KO) in the regulation of GABA release dynamics. Using patch-clamp recordings in hippocampal slices, we demonstrate that the lack of SynI impairs synchronous GABA release via a reduction of the readily releasable SVs and, in parallel, increases asynchronous GABA release. The effects of SynI deletion on synchronous GABA release were occluded by ω-AgatoxinIVA, indicating the involvement of P/Q-type Ca2+channel-expressing neurons. Using in situ hybridization, we show that SynI is more expressed in parvalbumin (PV) interneurons, characterized by synchronous release, than in cholecystokinin or SOM interneurons, characterized by a more asynchronous release. Optogenetic activation of PV and SOM interneurons revealed a specific reduction of synchronous release in PV/SynIKO interneurons associated with an increased asynchronous release in SOM/SynIKO interneurons. The results demonstrate that SynI is differentially expressed in interneuron subpopulations, where it boosts synchronous and limits asynchronous GABA release.


1999 ◽  
Vol 106 (4) ◽  
pp. 363-369 ◽  
Author(s):  
Catherine P. Scott-Taggart ◽  
Owen R. Van Cauwenberghe ◽  
Michael D. McLean ◽  
Barry J. Shelp

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