An inhibitor of glutamate decarboxylase and an antagonist of GAMMA-AMINOBUTYRIC ACID. It is used to induce convulsions in experimental animals.
Involuntary shock-like contractions, irregular in rhythm and amplitude, followed by relaxation, of a muscle or a group of muscles. This condition may be a feature of some CENTRAL NERVOUS SYSTEM DISEASES; (e.g., EPILEPSY, MYOCLONIC). Nocturnal myoclonus is the principal feature of the NOCTURNAL MYOCLONUS SYNDROME. (From Adams et al., Principles of Neurology, 6th ed, pp102-3).
'Allyl compounds' are organic substances that contain the allyl group (CH2=CH-CH2-) as a functional component, which can be found in various forms such as allyl alcohol, allyl chloride, and allyl esters.

Different effects of trypsin inhibitors on intestinal gene expression of secretin and on pancreatic bicarbonate secretion in CCK-A-receptor-deficient rats. (1/16)

The effects of oral administration of two synthetic trypsin inhibitors (camostate and ONO-3403) and soybean trypsin inhibitor (SBTI) on cholecystokinin (CCK), secretin gene expression and pancreatic secretion were examined in CCK-A-receptor-deficient (OLETF) rats. The rats were fed chow containing 0.1% trypsin inhibitors for 7 days. To examine pancreatic secretion, the rats were prepared with cannulae to drain the bile and pancreatic juice separately, a duodenal cannula and an external jugular vein cannula. The animals were maintained in Bollman cages and the experiments were conducted 4 days after surgery. The levels of CCK mRNA were significantly increased by each treatment. The levels of secretin mRNA were significantly increased by camostate and SBTI, but not by ONO-3403. Bicarbonate secretion was significantly increased in rats treated with camostate and ONO-3403, but not SBTI, while protein secretion was not affected by any treatment. These observations suggest that increased bicarbonate secretion produced by synthetic trypsin inhibitors in CCK-A-receptor-deficient rats may not be due to secretin but due to ONO-3403 in the circulation.  (+info)

Conversion into GABA (gamma-aminobutyric acid) may reduce the capacity of L-glutamine as an insulin secretagogue. (2/16)

We have carried out a detailed examination of L-glutamine metabolism in rat islets in order to elucidate the paradoxical failure of L-glutamine to stimulate insulin secretion. L-Glutamine was converted by isolated islets into GABA (gamma-aminobutyric acid), L-aspartate and L-glutamate. Saturation of the intracellular concentrations of all of these amino acids occurred at approx. 10 mmol/l L-glutamine, and their half-maximal values were attained at progressively increasing concentrations of L-glutamine (0.3 mmol/l for GABA; 0.5 and 1.0 mmol/l for Asp and Glu respectively). GABA accumulation accounted for most of the 14CO2 produced at various L-[U-14C]glutamine concentrations. Potentiation by L-glutamine of L-leucine-induced insulin secretion in perifused islets was suppressed by malonic acid dimethyl ester, was accompanied by a significant decrease in islet GABA accumulation, and was not modified in the presence of GABA receptor antagonists [50 micromol/l saclofen or 10 micromol/l (+)-bicuculline]. L-Leucine activated islet glutamate dehydrogenase activity, but had no effect on either glutamate decarboxylase or GABA transaminase activity, in islet homogenates. We conclude that (i) L-glutamine is metabolized preferentially to GABA and L-aspartate, which accumulate in islets, thus preventing its complete oxidation in the Krebs cycle, which accounts for its failure to stimulate insulin secretion; (ii) potentiation by L-glutamine of L-leucine-induced insulin secretion involves increased metabolism of L-glutamate and GABA via the Krebs cycle (glutamate dehydrogenase activation) and the GABA shunt (2-oxoglutarate availability for GABA transaminase) respectively, and (iii) islet release of GABA does not seem to play an important role in the modulation of the islet secretory response to the combination of L-leucine and L-glutamine.  (+info)

Cyclic dermorphin tetrapeptide analogues obtained via ring-closing metathesis. (3/16)

The dermorphin-derived cyclic tetrapeptide analogues H-Tyr-c[D-Cys-Phe-Cys]NH(2) and H-Tyr-c[D-Cys-Phe-D-Cys]NH(2) are opioid agonists at the mu and delta receptor. To enhance the metabolic stability of these peptides, we replaced the disulfide bridge with a bis-methylene moiety. This was achieved by solid-phase synthesis of the linear precursor peptide containing allylglycine residues in place of the Cys residues, followed by ring-closing metathesis. In the case of the peptide with L-configuration in the 4-position both the cis and the trans isomer of the resulting olefinic peptides were formed, whereas the cis isomer only was obtained with the peptide having the D-configuration in position 4. Catalytic hydrogenation yielded the saturated -CH(2)-CH(2)- bridged peptides. In comparison with the cystine-containing parent peptides, all olefinic peptides showed significantly reduced mu and delta agonist potencies in the guinea pig ileum and mouse vas deferens assays. The -CH(2)-CH(2)-bridged peptide with l-configuration in the 4-position was equipotent with its cystine-containing parent in both assays, whereas the bis-methylene analogue with D-configuration in position 4 was 10-27-fold less potent compared to its parent. The effect of the disulfide replacements with the -CH=CH- and -CH(2)-CH(2)- moieties on the conformational behavior of these peptides was examined by theoretical conformational analysis which provided plausible explanations in terms of structural parameters for the observed changes in opioid activity.  (+info)

Panic-prone state induced in rats with GABA dysfunction in the dorsomedial hypothalamus is mediated by NMDA receptors. (4/16)

Rats with chronic inhibition of GABA synthesis and consequently enhanced glutamatergic excitation in the dorsomedial hypothalamus (DMH) develop panic-like responses, defined as tachycardia, tachypnea, hypertension, and increased anxiety as measured by a social interaction (SI) test, after intravenous sodium lactate infusions, a phenomenon similar to patients with panic disorder. Therefore, the present studies tested the role of the postsynaptic NMDA and AMPA type glutamatergic receptors in the lactate-induced panic-like responses in these rats. Rats were fit with femoral arterial and venous catheters and Alzet pumps [filled with the GABA synthesis inhibitor L-allylglycine (L-AG; 3.5 nmol/0.5 microl per hour) or its inactive isomer D-AG] into the DMH. After 4-5 d of recovery only those rats with L-AG pumps exhibited panic-like responses to lactate infusions. Using double immunocytochemistry, we found that rats exhibiting panic-like responses (e.g., L-AG plus lactate) had increased c-Fos immunoreactivity in DMH neurons expressing the NMDA receptor 1 (NR1) subunit, but not those expressing the glutamate receptor 2 and 3 subunits of the AMPA receptors. To confirm this pharmacologically, we tested another group of rats implanted with l-AG pumps with intravenous lactate infusions preceded by injections of either NMDA [aminophosphonopentanoic acid (AP-5) or (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine maleate (MK-801)] or non-NMDA [CNQX or 4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodazepin-5-yl)-benzenamine dihydrochloride (GYKI52466)] antagonists into the DMH. Injections of NMDA, but not non-NMDA, antagonists into the DMH resulted in dose-dependent blockade of the tachycardia, tachypnea, hypertension, and SI responses after lactate infusions. These results suggest that NMDA, and not non-NMDA, type glutamate receptors regulate lactate-induced panic-like responses in rats with GABA dysfunction in the DMH.  (+info)

Neural pathways underlying lactate-induced panic. (5/16)

Panic disorder is a severe anxiety disorder characterized by susceptibility to induction of panic attacks by subthreshold interoceptive stimuli such as 0.5 M sodium lactate infusions. Although studied for four decades, the mechanism of lactate sensitivity in panic disorder has not been understood. The dorsomedial hypothalamus/perifornical region (DMH/PeF) coordinates rapid mobilization of behavioral, autonomic, respiratory and endocrine responses to stress, and rats with disrupted GABA inhibition in the DMH/PeF exhibit panic-like responses to lactate, similar to panic disorder patients. Utilizing a variety of anatomical and pharmacological methods, we provide evidence that lactate, via osmosensitive periventricular pathways, activates neurons in the compromised DMH/PeF, which relays this signal to forebrain limbic structures such as the bed nucleus of the stria terminalis to mediate anxiety responses, and specific brainstem sympathetic and parasympathetic pathways to mediate the respiratory and cardiovascular components of the panic-like response. Acutely restoring local GABAergic tone in the DMH/PeF blocked lactate-induced panic-like responses. Autonomic panic-like responses appear to be a result of DMH/PeF-mediated mobilization of sympathetic responses (verified with atenolol) and resetting of the parasympathetically mediated baroreflex. Based on our findings, DMH/PeF efferent targets such as the C1 adrenergic neurons, paraventricular hypothalamus, and the central amygdala are implicated in sympathetic mobilization; the nucleus of the solitary tract is implicated in baroreflex resetting; and the parabrachial nucleus is implicated in respiratory responses. These results elucidate neural circuits underlying lactate-induced panic-like responses and the involvement of both sympathetic and parasympathetic systems.  (+info)

Disruption of GABAergic tone in the dorsomedial hypothalamus attenuates responses in a subset of serotonergic neurons in the dorsal raphe nucleus following lactate-induced panic. (6/16)

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Low modularity of aminoacyl-tRNA substrates in polymerization by the ribosome. (7/16)

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Modelling of tumour--host coexistence In vitro in the presence of serine protease inhibitors. (8/16)

The activities of cell surface serine proteases are markedly enhanced in malignant tumours. Proteolytic degradation of the extracellular matrix and basal membrane of normal cells is an important event for tumour cell growth and invasion. Two well-known broad-spectrum inhibitors of serine protease, Foy-305 and Ono-3403, were evaluated for their ability to affect the growth rate and survival of MCF7 breast cancer cells co-cultured with MRC5 lung fibroblasts as feeder cells in the absence of serum. Flow cytometry and differential staining demonstrated that in the mixed culture, the rate of tumor growth was dependent upon the presence of the feeder MRC5 lung fibroblasts and could be obviated by the additional presence of the inhibitors of serine proteases.  (+info)

Allylglycine is not a medical term, but it is a chemical compound used in organic synthesis. It is an amino acid with the formula CH2=CH-CH2-CONH-CH2-COOH. Allylglycine is not naturally occurring and is typically produced in the laboratory for use as a building block in the synthesis of other compounds.

In the context of medicine, allylglycine may be used in research or in the development of new drugs, but it is not a medication or treatment that is used directly in patients.

Myoclonus is a medical term that describes a quick, involuntary jerking muscle spasm. These spasms can happen once or repeat in a series, and they can range from mild to severe in nature. Myoclonus can affect any muscle in the body and can be caused by several different conditions, including certain neurological disorders, injuries, or diseases. In some cases, myoclonus may occur without an identifiable cause.

There are various types of myoclonus, classified based on their underlying causes, patterns of occurrence, and associated symptoms. Some common forms include:

1. Action myoclonus: Occurs during voluntary muscle movements
2. Stimulus-sensitive myoclonus: Triggered by external or internal stimuli, such as touch, sound, or light
3. Physiological myoclonus: Normal muscle jerks that occur during sleep onset (hypnic jerks) or during sleep (nocturnal myoclonus)
4. Reflex myoclonus: Result of a reflex arc activation due to a peripheral nerve stimulation
5. Epileptic myoclonus: Part of an epilepsy syndrome, often involving the brainstem or cortex
6. Symptomatic myoclonus: Occurs as a result of an underlying medical condition, such as metabolic disorders, infections, or neurodegenerative diseases

Treatment for myoclonus depends on the specific type and underlying cause. Medications, physical therapy, or lifestyle modifications may be recommended to help manage symptoms and improve quality of life.

Allyl compounds are organic compounds that contain the allyl group, which is a functional group with the formula CH2=CH-CH2-. The allyl group consists of a methylene bridge (CH2-) flanked by a carbon-carbon double bond (-CH=). Allyl compounds can be derived from allyl alcohol, allyl chloride, or other allyl halides and can participate in various chemical reactions due to the reactivity of the double bond. They are used in organic synthesis, pharmaceuticals, and agrochemicals.

... is known to induce seizures in animals studies, presumably due to this GDC-inhibiting activity. 3- ... Allylglycine is a glycine derivative. It is an inhibitor of glutamate decarboxylase. Inhibition of glutamate decarboxylase ... Abshire VM, Hankins KD, Roehr KE, DiMicco JA (November 1988). "Injection of L-allylglycine into the posterior hypothalamus in ... Thomas J, Yang YC (June 1991). "Allylglycine induced seizures in male and female rats". Physiol. Behav. 49 (6): 1181-3. doi: ...
Allylglycine Thiolactic acid (2-mercaptopropionic acid) Horton, R. W; Meldrum, B. S (1973). "Seizures induced by allylglycine, ... It has higher potency and faster onset of action compared to allylglycine. It is used to prepare hydrophilic gold nanoparticles ...
3-Mercaptopropionic acid Allylglycine Glycine receptor antagonists are drugs which inactivates the glycine receptors. ...
... a metabolite of allylglycine". J Neurochem. 32 (3): 907-13. doi:10.1111/j.1471-4159.1979.tb04574.x. PMID 430066. S2CID 31823191 ...
Atmuri, N. D. P.; Lubell, W. D. (2015). "Preparation of N-(Boc)-Allylglycine Methyl Ester Using a Zinc-mediated, Palladium- ...
Kunz DA, Ribbons DW, Chapman PJ (1981). "Metabolism of allylglycine and cis-crotylglycine by Pseudomonas putida (arvilla) mt-2 ...
Kunz DA, Ribbons DW, Chapman PJ (1981). "Metabolism of allylglycine and cis-crotylglycine by Pseudomonas putida (arvilla) mt-2 ...
L-Allylglycine and N-BOC-l-Allylglycine". Organic Syntheses. 76: 57. doi:10.15227/orgsyn.076.0057. White, James D.; Kranemann, ...
L-Allylglycine and N-BOC-l-Allylglycine". Organic Syntheses. 76: 57. doi:10.15227/orgsyn.076.0057. (Articles without InChI ...
... allylglycine MeSH D12.125.481.700 - n-substituted glycines MeSH D12.125.481.700.249 - glycocholic acid MeSH D12.125.481.700. ...
The molecular formula C5H9NO2 (molar mass : 115.13 g/mol) may refer to: Allylglycine (+)-cis-2-Aminomethylcyclopropane ...
... allylglycine MeSH D02.455.326.271.122.272 - allylisopropylacetamide MeSH D02.455.326.271.367 - ethylenes MeSH D02.455.326.271. ...
Allylglycine is known to induce seizures in animals studies, presumably due to this GDC-inhibiting activity. 3- ... Allylglycine is a glycine derivative. It is an inhibitor of glutamate decarboxylase. Inhibition of glutamate decarboxylase ... Abshire VM, Hankins KD, Roehr KE, DiMicco JA (November 1988). "Injection of L-allylglycine into the posterior hypothalamus in ... Thomas J, Yang YC (June 1991). "Allylglycine induced seizures in male and female rats". Physiol. Behav. 49 (6): 1181-3. doi: ...
Allylglycine / metabolism * Bacterial Proteins / chemistry* * Bacterial Proteins / genetics * Bacterial Proteins / isolation & ...
This concept is supported by the finding that the pattern of brain damage in animals with repetitive seizures induced by allyl glycine ...
92. ALLYLGLYCINE [ԱԼԻԼԳԼԻՑԻՆ] 43. ALDOSTERONE [ԱԼԴՈՍՏԵՐՈՆ] 93. ALLYLISOPROPYLACETAMIDE [ԱԼԻԼԻԶՈՊՐՈՊԻԼԱՑԵՏԱՄԻԴ] 44. ALDOSTERONE ...
Enantiomerically enriched allylglycine derivatives through the catalytic asymmetric allylation of iminoesters and ...
... on decay of the intermediate and production of l-allylglycine in the reaction with 4,4,5,5-[2H4]-l-Lys suggest that the ... and 4-chloro-l-allylglycine and can analogously fragment l-Lys itself. BesC belongs to the emerging family of O2-activating non ...
2-Amino-4-Pentenoic Acid use Allylglycine 2-Amino-4,5,6,7-tetrahydro-6-propylaminobenzothiazole use Pramipexole ...
2-Amino-4-Pentenoic Acid use Allylglycine 2-Amino-4,5,6,7-tetrahydro-6-propylaminobenzothiazole use Pramipexole ...
In baboons pretreated with allylglycine, 170--185 mg/kg, a similar but briefer protection was induced by clobazam. Neurological ...
Allylglycine Preferred Term Term UI T001470. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1980). ... Allylglycine Preferred Concept UI. M0000753. Registry Number. 1069-48-3. Scope Note. An inhibitor of glutamate decarboxylase ... Allylglycine. Tree Number(s). D02.455.326.271.122.260. D12.125.481.100. Unique ID. D000501. RDF Unique Identifier. http://id. ...
Allylglycine Preferred Term Term UI T001470. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1980). ... Allylglycine Preferred Concept UI. M0000753. Registry Number. 1069-48-3. Scope Note. An inhibitor of glutamate decarboxylase ... Allylglycine. Tree Number(s). D02.455.326.271.122.260. D12.125.481.100. Unique ID. D000501. RDF Unique Identifier. http://id. ...
This concept is supported by the finding that the pattern of brain damage in animals with repetitive seizures induced by allyl glycine ...
Allylglycine - Preferred Concept UI. M0000753. Scope note. An inhibitor of glutamate decarboxylase and an antagonist of GAMMA- ...
Allura Red AC Dye N0000007521 Allyl Compounds N0000007522 Allylamine N0000167406 Allylestrenol N0000170215 Allylglycine ...
GABA AGENTS ALLYLGLYCINE GABA AGENTS ALPRAZOLAM GABA AGENTS AMINOOXYACETIC ACID GABA AGENTS AMOBARBITAL GABA AGENTS BACLOFEN ... GABA AGONISTS ALLYLGLYCINE GABA ANTAGONISTS BICUCULLINE GABA ANTAGONISTS CLOZAPINE GABA ANTAGONISTS GABA ANTAGONISTS GABA ... NEUROTRANSMITTER AGENTS ALLYLGLYCINE NEUROTRANSMITTER AGENTS ALPHA-AMINO-3-HYDROXY-5-METHYL-4-ISOXAZ NEUROTRANSMITTER AGENTS ... NEUROTRANSMITTERS AND NEUROTRANSMITTER ALLYLGLYCINE NEUROTRANSMITTERS AND NEUROTRANSMITTER ALPHA-AMINO-3-HYDROXY-5-METHYL-4- ...
These were synthesized in good yields (45-75%) from the common starting material (S)-allylglycine obtained by asymmetric ...
Horton, R.W.; Meldrum, B.S. 1973: Seizures induced by allylglycine, 3-mercaptopropionic acid and 4-deoxypyridoxine in mice and ...

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