scholarly journals HISTOCHEMICAL LOCALIZATION OF BRAIN SUCCINIC SEMIALDEHYDE DEHYDROGENASE-A γ-AMINOBUTYRIC ACID DEGRADATIVE ENZYME

1971 ◽  
Vol 19 (7) ◽  
pp. 405-415 ◽  
Author(s):  
K. L. SIMS ◽  
H. A. WEITSEN ◽  
F. E. BLOOM
Keyword(s):  
Succinic Acid ◽  
Direct Reduction ◽  
Dendritic Tree ◽  
Nordihydroguaiaretic Acid ◽  
Pyridine Nucleotide ◽  
Aminobutyric Acid ◽  
Succinic Semialdehyde ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Acid Dehydrogenase ◽  
Semialdehyde Dehydrogenase

Succinic semialdehyde dehydrogenase is the final enzyme in the degradative pathway of γ-aminobutyric acid, a postulated inhibitory synaptic transmitter. This study reports a specific, sensitive technique for the localization of succinic semialdehyde dehydrogenase in rat brain. The technique utilizes the direct reduction of nitroblue tetrazolium by reduced pyridine nucleotide at an alkaline pH, a mechanism of formazan production substantiated by biochemical studies. The succinic semialdehyde dehydrogenase histochemical reaction is completely inhibited by p-hydroxybenzaldehyde and m-hydroxybenzaldehyde, compounds which have no effect on succinic acid dehydrogenase and reduced diphosphopyridine nucleotide diaphorase. Conversely, succinic acid dehydrogenase and reduced diphosphopyridine nucleotide diaphorase are inhibited by malonate and nordihydroguaiaretic acid, respectively, substances which have no effect on succinic semialdehyde dehydrogenase. The distribution and intensity of staining for succinic semialdehyde dehydrogenase are different from that seen following the succinic acid dehydrogenase and reduced diphosphopyridine nucleotide diaphorase reactions and can be localized to groups of neurons and their cell processes, e.g., the Purkinje cell dendritic tree, and in specific regions of neuropil.

Host Gamma Aminobutyric Acid Metabolic Pathway is involved in Resistance against Rhizoctonia solani

2020 ◽  
Author(s):  
Mamta Rani ◽  
Gopaljee Jha
Keyword(s):  
Gene Silencing ◽  
Rhizoctonia Solani ◽  
Fungal Pathogen ◽  
Large Scale ◽  
Aminobutyric Acid ◽  
Primary Metabolism ◽  
Succinic Semialdehyde ◽  
Gamma Aminobutyric Acid ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Semialdehyde Dehydrogenase

Rhizoctonia solani is a highly destructive necrotrophic fungal pathogen having a diverse host range, including rice and tomato. Previously R. solani infection in rice has been found to cause large-scale readjustment in host primary metabolism and accumulation of various stress associated metabolites such as gamma aminobutyric acid (GABA). In this study, we report upregulation of GABA shunt genes during pathogenesis of R. solani in rice as well as tomato. The exogenous application of GABA provided partial resistance against R. solani infection in both the hosts. Further, using virus induced gene silencing (VIGS) approach, we knocked down the expression of some of the tomato genes involved in GABA biosynthesis (glutamate decarboxylase; GAD) and GABA catabolism (GABA-transaminase; GABA-T and succinic semialdehyde dehydrogenase; SSADH) to study their role in host defense against R. solani infection. The silencing of each of these genes was found to enhance disease susceptibility in tomato. Overall the results from gene expression analysis, exogenous chemical treatment and gene silencing studies suggest that GABA pathway plays a positive role in plant resistance against necrotrophic fungal pathogen R. solani.

scholarly journals Characterization of Genes Involved in γ-Aminobutyric Acid Metabolic Pathways Response to Metabolites Accumulation in Embryos during Barley Germination

2021 ◽  
Vol 25 (04) ◽  
pp. 786-794
Author(s):  
Mengyuan Jin
Keyword(s):  
Gene Expression ◽  
Metabolic Pathways ◽  
Aminobutyric Acid ◽  
Acid Decarboxylase ◽  
Succinic Semialdehyde ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Semialdehyde Dehydrogenase ◽  
Key Enzyme ◽  
Gaba Content ◽  
Gaba Accumulation

To reveal the key enzyme genes involved in γ-aminobutyric acid (GABA) metabolic pathways response to elevated metabolite storage in embryos during barley germination, this study investigated the GABA content, cloned GABA metabolic pathway genes and analyzed their expression levels, respectively. In barley embryos, GABA content continued to rise during the soaking process and then decreased after the germination. Three genes including glutamic acid decarboxylase (GAD), GABA transaminase (GABA-T) and succinic semialdehyde dehydrogenase (SSADH) involved in the GABA pathway were cloned and characterized from the barley embryos, respectively. Before the germination, the expression of GAD gene was up-regulated, while GABA-T gene expression was down-regulated. After the germination, GAD gene expression was lowered, but GABA-T gene expression was rapidly increased. The SSADH gene expression remained stable after soaking of 4 h, and then down-regulated. There is evidence that the high GABA content in germinating barley seeds is parallel with the upregulation of the GAD gene, and down-regulation of GABA-T gene. These results indicate that the expression level of the genes involved in GABA pathway is a crucial factor in GABA accumulation during soaking and germination. This study is beneficial for the development of GABA-rich barley products by germination. © 2021 Friends Science Publishers

scholarly journals THE METABOLISM OF GAMMA AMINOBUTYRIC ACID IN THE LOBSTER NERVOUS SYSTEM

1970 ◽  
Vol 46 (2) ◽  
pp. 290-299 ◽  
Author(s):  
Z. W. Hall ◽  
M. D. Bownds ◽  
E. A. Kravitz
Keyword(s):  
Aminobutyric Acid ◽  
Inhibitory Neurons ◽  
Decarboxylase Activity ◽  
Succinic Semialdehyde ◽  
Gamma Aminobutyric Acid ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Gaba Metabolism ◽  
Semialdehyde Dehydrogenase ◽  
Electrophoretic Behavior ◽  
Inhibitory Transmitter

γ-aminobutyric acid (GABA) is the inhibitory transmitter compound at the lobster neuromuscular junction. This paper presents a comparison of the enzymes of GABA metabolism in single identified inhibitory and excitatory axons from lobster walking legs. Inhibitory axons contain more than 100 times as much glutamic decarboxylase activity as do excitatory axons. GABA-glutamic transaminase is found in both excitatory and inhibitory axons, but about 50% more enzyme is present in inhibitory axons. The kinetic and electrophoretic behavior of the transaminase activity in excitatory and inhibitory axons is similar. Succinic semialdehyde dehydrogenase is found in both axon types, as is an unknown enzyme which converts a contaminant in radioactive glutamic acid to GABA. In lobster inhibitory neurons, therefore, the ability to accumulate GABA ultimately rests on the ability of the neuron to accumulate the enzyme glutamic decarboxylase.

Mutation analysis and prenatal diagnosis in a Chinese family with succinic semialdehyde dehydrogenase and a systematic review of the literature of reported ALDH5A1 mutations

2016 ◽  
Vol 44 (4) ◽  
Author(s):  
Ning Liu ◽  
Xiang-dong Kong ◽  
Quan-cheng Kan ◽  
Hui-rong Shi ◽  
Qing-hua Wu ◽  
...  
Keyword(s):  
Systematic Review ◽  
Prenatal Diagnosis ◽  
Genetic Analysis ◽  
Aminobutyric Acid ◽  
Chinese Family ◽  
Succinic Semialdehyde ◽  
Review Of The Literature ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Semialdehyde Dehydrogenase ◽  
Ssadh Deficiency

AbstractSuccinic semialdehyde dehydrogenase (SSADH) deficiency is a neurometabolic disease in which the degradation of γ-aminobutyric acid (GABA) is impaired. The purpose of this study was to report two novelGenetic analysis ofTwo novel

scholarly journals The metabolism of succinic semialdehyde by a psychrophilic basidiomycete

1969 ◽  
Vol 47 (5) ◽  
pp. 809-813 ◽  
Author(s):  
Parker N. Davies ◽  
Gary A. Strobel
Keyword(s):  
Substrate Specificity ◽  
Succinic Acid ◽  
Crude Extract ◽  
Major Portion ◽  
Succinic Semialdehyde ◽  
Ph Optimum ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Coenzyme Specificity ◽  
Semialdehyde Dehydrogenase

A plant-pathogenic psychrophilic basidiomycete metabolized succinic semialdehyde-14C to 14CO2 and various compounds labelled with 14C that appeared in the cation, anion, and neutral fractions of the fungus. The major portion of succinic semialdehyde taken into the cell was oxidized to succinic acid. A crude extract of the fungus possessed a soluble succinic semialdehyde dehydrogenase that was characterized as to stability, pH optimum, Km, substrate specificity, and coenzyme specificity. Electrophoresis of the crude extract on acrylamide gels showed that there were either several enzymes able to oxidize succinic semialdehyde or that several forms of the same enzyme exist in the fungus.

scholarly journals A Randomized Controlled Trial of SGS-742, a γ-aminobutyric acid B (GABA-B) Receptor Antagonist, for Succinic Semialdehyde Dehydrogenase Deficiency

2021 ◽  
pp. 088307382110128
Author(s):  
John M. Schreiber ◽  
Edythe Wiggs ◽  
Rose Cuento ◽  
Gina Norato ◽  
Irene H. Dustin ◽  
...  
Keyword(s):  
Adaptive Behavior ◽  
Magnetic Stimulation ◽  
Dehydrogenase Deficiency ◽  
Assessment Scale ◽  
Aminobutyric Acid ◽  
Behavior Assessment ◽  
Succinic Semialdehyde ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Semialdehyde Dehydrogenase ◽  
Succinic Semialdehyde Dehydrogenase Deficiency

We examined safety, tolerability, and efficacy of SGS-742, a γ-aminobutyric acid B (GABA-B) receptor antagonist, in patients with succinic semialdehyde dehydrogenase deficiency. This was a single-center randomized, double-blind crossover phase II clinical trial of SGS-742 versus placebo in patients with succinic semialdehyde dehydrogenase deficiency. Procedures included transcranial magnetic stimulation and the Adaptive Behavior Assessment Scale. Nineteen subjects were consented and enrolled; the mean age was 14.0 ± 7.5 years and 11 (58%) were female. We did not find a significant effect of SGS-742 on the Adaptive Behavior Assessment Scale score, motor threshold, and paired-pulse stimulation. The difference in recruitment curve slopes between treatment groups was 0.003 ( P = .09). There was no significant difference in incidence of adverse effects between drug and placebo arms. SGS-742 failed to produce improved cognition and normalization of cortical excitability as measured by the Adaptive Behavior Assessment Scale and transcranial magnetic stimulation. Our data do not support the current use of SGS-742 in succinic semialdehyde dehydrogenase deficiency. Trial registry number NCT02019667. Phase 2 Clinical Trial of SGS-742 Therapy in Succinic Semialdehyde Dehydrogenase Deficiency. https://clinicaltrials.gov/ct2/show/NCT02019667

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