Inhibitors of crayfish glutamic acid decarboxylase

Grossfeld, Robert M.; Yancey, Steven W.; Baxter, Claude F.

doi:10.1007/bf00964526

Cited by 12 publications

(3 citation statements)

References 36 publications

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“…NMRS analyses of cerebrum extracts showed that the reduced concentrations of GABA were caused by decreased neuronal synthesis of GABA from glucose, indicating that the process is affected by changes in the number of synaptic vesicles. The steady-state concentration of GABA in vivo is primarily regulated by GAD activity (Roberts and Simonsen 1963;Martin and Rimvall 1993;Battaglioli et al 2003), and previous studies have shown that increased cytosolic concentrations of GABA can down-regulate its own synthesis through feedback inhibition of GAD (Grossfeld et al 1984;Porter and Martin 1984;Rimvall and Martin 1994;Battaglioli et al 2003). The protein level of GAD (Rosahl et al 1995), and GAD activity measured at optimal conditions in vitro, were similar in cerebrum homogenates from synapsin DKO and wild-type mice (unpublished results).…”

Section: Discussionmentioning

confidence: 55%

Distinct changes in neuronal and astrocytic amino acid neurotransmitter metabolism in mice with reduced numbers of synaptic vesicles

Bogen

Risa

Haug

et al. 2008

Journal of Neurochemistry

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The relations between glutamate and GABA concentrations and synaptic vesicle density in nerve terminals were examined in an animal model with 40–50% reduction in synaptic vesicle numbers caused by inactivation of the genes encoding synapsin I and II. Concentrations and synthesis of amino acids were measured in extracts from cerebrum and a crude synaptosomal fraction by HPLC and 13C nuclear magnetic resonance spectroscopy (NMRS), respectively. Analysis of cerebrum extracts, comprising both neurotransmitter and metabolic pools, showed decreased concentration of GABA, increased concentration of glutamine and unchanged concentration of glutamate in synapsin I and II double knockout (DKO) mice. In contrast, both glutamate and GABA concentrations were decreased in crude synaptosomes isolated from synapsin DKO mice, suggesting that the large metabolic pool of glutamate in the cerebral extracts may overshadow minor changes in the transmitter pool. 13C NMRS studies showed that the changes in amino acid concentrations in the synapsin DKO mice were caused by decreased synthesis of GABA (20–24%) in cerebral neurons and increased synthesis of glutamine (36%) in astrocytes. In a crude synaptosomal fraction, the glutamate synthesis was reduced (24%), but this reduction could not be detected in cerebrum extracts. We suggest that lack of synaptic vesicles causes down‐regulation of neuronal GABA and glutamate synthesis, with a concomitant increase in astrocytic synthesis of glutamine, in order to maintain normal neurotransmitter concentrations in the nerve terminal cytosol.

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Section: Discussionmentioning

confidence: 55%

Distinct changes in neuronal and astrocytic amino acid neurotransmitter metabolism in mice with reduced numbers of synaptic vesicles

Bogen

Risa

Haug

et al. 2008

Journal of Neurochemistry

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“…To test this possibility, five different compounds, presumed to play a role as either a substrate analogue or an antagonist in the GDAR system, were selected. These include 3-mercaptopropionic acid, which is an analogue of glutamate, and the other four, including aminooxyacetic acid, 4-deoxypyridoxine hydrochloride, isoniazid, and thiosemicarbazide, are antagonists of pyridoxal phosphate, a cofactor of GadA and GadB [ 35 - 42 ]. The concentrations of tested compounds were determined by measuring the maximal concentrations with no growth inhibitory effects at pH 7.0: 3-mercaptopropionic acid at 0.5 mM, aminooxyacetic acid at 0.02 mM, 4-deoxypyridoxine hydrochloride at 1 mM, isoniazid at 1 mM, and thiosemicarbazide at 0.2 mM.…”

Section: Resultsmentioning

confidence: 99%

Cooperative Interaction between Acid and Copper Resistance in Escherichia coli

Kim

Lee

Park

et al. 2022

J. Microbiol. Biotechnol.

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The persistence of pathogenic Escherichia coli under acidic conditions poses a serious risk to food safety, especially in acidic foods such as kimchi. To identify the bacterial factors required for acid resistance, transcriptomic analysis was conducted on an acid-resistant enterotoxigenic E. coli strain and the genes with significant changes in their expression under acidic pH were selected as putative resistance factors against acid stress. These genes included those associated with a glutamatedependent acid resistance (GDAR) system and copper resistance. E. coli strains lacking GadA, GadB, or YbaST, the components of the GDAR system, exhibited significantly attenuated growth and survival under acidic stress conditions. Accordantly, the inhibition of the GDAR system by 3-mercaptopropionic acid and aminooxyacetic acid abolished bacterial adaptation and survival under acidic conditions, indicating the indispensable role of a GDAR system in acid resistance. Intriguingly, the lack of cueR encoding a transcriptional regulator for copper resistance genes markedly impaired bacterial resistance to acid stress as well as copper. Conversely, the absence of YbaST severely compromised bacterial resistance against copper, suggesting an interplay between acid and copper resistance. These results suggest that a GDAR system can be a promising target for developing control measures to prevent E. coli resistance to acid and copper treatments.

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“…Besides glucose, glutamic acid is the only compound used for brain fuel. The brain converts glutamic acid to a compound that regulates brain cell activity (Grossfeld et al 1984). Glutamic acid increases the firing of neurons in the nervous system.…”

Section: Introductionmentioning

confidence: 99%

Studies on in vitro release of CPM from semi-interpenetrating polymer network (IPN) composed of chitosan and glutamic acid

Kumari

Kundu

2008

Bull Mater Sci

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Interpenetrating polymer network (IPN) beads consisting of chitosan-glutamic acid were prepared for in vitro study of controlled release of chlorpheniramine maleate (CPM). A viscous solution of chitosanglutamic acid was prepared in 2% acetic acid solution, extruded as droplets through a syringe to alkalimethanol solution and the precipitated beads were crosslinked using glutaraldehyde solution. Swelling and drug release studies were carried out. Transport of release medium through the semi-IPN depended upon its pH and extent of crosslinking. The structural and morphological studies of beads were carried out by using a scanning electron microscope (SEM). The larger surface area of beads as well as their ease of handling makes them ideal agents of controlled release.

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Inhibitors of crayfish glutamic acid decarboxylase

Cited by 12 publications

References 36 publications

Distinct changes in neuronal and astrocytic amino acid neurotransmitter metabolism in mice with reduced numbers of synaptic vesicles

Distinct changes in neuronal and astrocytic amino acid neurotransmitter metabolism in mice with reduced numbers of synaptic vesicles

Cooperative Interaction between Acid and Copper Resistance in Escherichia coli

Studies on in vitro release of CPM from semi-interpenetrating polymer network (IPN) composed of chitosan and glutamic acid

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