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 ...
... a metabolite of allylglycine". J Neurochem. 32 (3): 907-13. doi:10.1111/j.1471-4159.1979.tb04574.x. PMID 430066. S2CID 31823191 ...
Allylglycine Methyl Ester Using a Zinc-mediated, Palladium-catalyzed Cross-coupling Reaction". Org. Synth. 92: 103. doi: ...
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 ...
Sinomenine TBPO TBPS Tetramethylenedisulfotetramine Thujone GABA synthesis inhibitors 3-Mercaptopropionic acid Allylglycine ...
... 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 ...
... 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: ...
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...
In 2001, the German Federal Institute for Risk Assessment (Bundesinstitut für Risikobewertung, BfR) objected to the addition of isolated theanine to beverages.[39][40] The institute stated the amount of theanine consumed by regular drinkers of tea or coffee is virtually impossible to determine. While it was estimated the quantity of green tea consumed by the average Japanese tea drinker per day contains about 20 mg of the substance, there are no studies measuring the amount of theanine being extracted by typical preparation methods, or the percentage lost by discarding the first infusion. Therefore, with the Japanese being exposed to possibly much less than 20 mg per day, and Europeans presumably even less, it was the opinion of the BfR that pharmacological reactions to drinks typically containing 50 mg of theanine per 500 milliliters could not be excluded-reactions such as impairment of psychomotor skills and amplification of the sedating effects of alcohol and hypnotics.[41] In 2006, a study ...
GAD67 and GAD65 are also regulated differently post-translationally. Both GAD65 and GAD67 are regulated via phosphorylation of a dynamic catalytic loop,[10][11] but the regulation of these isoforms differs; GAD65 is activated by phosphorylation while GAD67 is inhibited by phosphorylation. GAD67 is predominantly found activated (~92%), whereas GAD65 is predominantly found inactivated (~72%).[12] GAD67 is phosphorylated at threonine 91 by protein kinase A (PKA), while GAD65 is phosphorylated, and therefore regulated by, protein kinase C (PKC). Both GAD67 and GAD65 are also regulated post-translationally by Pyridoxal 5'-phosphate (PLP); GAD is activated when bound to PLP and inactive when not bound to PLP.[12] Majority of GAD67 is bound to PLP at any given time, whereas GAD65 binds PLP when GABA is needed for neurotransmission.[12] This reflects the functional properties of the two isoforms; GAD67 must be active at all times for normal cellular functioning, and is therefore constantly activated by ...
Regulation of GS only occurs in prokaryotes.[24] GS is subject to reversible covalent modification. Tyr397 of all 12 subunits can undergo adenylylation or deadenylylation by adenylyl transferase (AT), a bifunctional regulatory enzyme.[24] Adenylylation is a post-translational modification involving the covalent attachment of AMP to a protein side chain. Each adenylylation requires an ATP and complete inhibition of GS requires 12 ATP. Deadenylylation by AT involves phosphorolytic removal of the Tyr-linked adenylyl groups as ADP. AT activity is influenced by the regulatory protein that is associated with it: PII, a 44-kD trimer.[24] PII also undergoes post-translational modification by uridylyl transferase, thus PII has two forms. The state of PII dictates the activity of adenylyl transferase. If PII is not uridylylated, then it will take on the PIIA form. The AT:PIIA complex will deactivate GS by adenylylation. If PII is uridylylated, then it will take on the PIID form. The AT:PIID complex will ...
Besides the nervous system, GABA is also produced at relatively high levels in the insulin-producing β-cells of the pancreas. The β-cells secrete GABA along with insulin and the GABA binds to GABA receptors on the neighboring islet α-cells and inhibits them from secreting glucagon (which would counteract insulin's effects).[25] GABA can promote the replication and survival of β-cells[26][27][28] and also promote the conversion of α-cells to β-cells, which may lead to new treatments for diabetes.[29] GABA has also been detected in other peripheral tissues including intestines, stomach, Fallopian tubes, uterus, ovaries, testes, kidneys, urinary bladder, the lungs and liver, albeit at much lower levels than in neurons or β-cells. GABAergic mechanisms have been demonstrated in various peripheral tissues and organs, which include the intestines, the stomach, the pancreas, the Fallopian tubes, the uterus, the ovaries, the testes, the kidneys, the urinary bladder, the lungs, and the liver.[30] ...
... (marketed as Depamide by Sanofi-Aventis) is a carboxamide derivative of valproic acid used in the treatment of epilepsy and some affective disorders. It is rapidly metabolised (80%) to valproic acid (another anticonvulsant) but has anticonvulsant properties itself. It may produce more stable plasma levels than valproic acid or sodium valproate and may be more effective at preventing febrile seizures. However, it is over one hundred times more potent as an inhibitor of liver microsomal epoxide hydrolase. This makes it incompatible with carbamazepine and can affect the ability of the body to remove other toxins. Valpromide is no safer during pregnancy than valproic acid. Valpromide is formed through the reaction of valproic acid and ammonia via an intermediate acid chloride. In pure form, valpromide is a white crystalline powder and has melting point 125-126 °C. It is practically insoluble in water but soluble in hot water. It is available on the market in some European countries. ...
... is an azo dye that is used as a dye-stuff. It is a direct dye for cotton textiles.[3] In biosciences, it is used as vital stain to selectively colour dead tissues or cells blue. Live cells or tissues with intact cell membranes are not coloured. Since cells are very selective in the compounds that pass through the membrane, in a viable cell trypan blue is not absorbed; however, it traverses the membrane in a dead cell. Hence, dead cells appear as a distinctive blue colour under a microscope. Since live cells are excluded from staining, this staining method is also described as a dye exclusion method. This dye may be a cause of certain birth defects, such as encephalocele.[citation needed] ...
Glutamate is the most abundant excitatory neurotransmitter in the vertebrate nervous system.[21] At chemical synapses, glutamate is stored in vesicles. Nerve impulses trigger release of glutamate from the presynaptic cell. Glutamate acts on ionotropic and metabotropic (G-protein coupled) receptors.[21] In the opposing postsynaptic cell, glutamate receptors, such as the NMDA receptor or the AMPA receptor, bind glutamate and are activated. Because of its role in synaptic plasticity, glutamate is involved in cognitive functions such as learning and memory in the brain.[22] The form of plasticity known as long-term potentiation takes place at glutamatergic synapses in the hippocampus, neocortex, and other parts of the brain. Glutamate works not only as a point-to-point transmitter, but also through spill-over synaptic crosstalk between synapses in which summation of glutamate released from a neighboring synapse creates extrasynaptic signaling/volume transmission.[23] In addition, glutamate plays ...
Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the adult vertebrate. Medium spiny cells are a typical example of inhibitory central nervous system GABAergic cells. In contrast, GABA exhibits both excitatory and inhibitory actions in insects, mediating muscle activation at synapses between nerves and muscle cells, and also the stimulation of certain glands.[4] In mammals, some GABAergic neurons, such as chandelier cells, are also able to excite their glutamatergic counterparts.[5] GABAA receptors are ligand-activated chloride channels: when activated by GABA, they allow the flow of chloride ions across the membrane of the cell. Whether this chloride flow is depolarizing (makes the voltage across the cell's membrane less negative), shunting (has no effect on the cell's membrane potential), or inhibitory/hyperpolarizing (makes the cell's membrane more negative) depends on the direction of the flow of chloride. When net ...
... is a non-selective and irreversible inhibitor of the enzyme monoamine oxidase (MAO). It inhibits both of the respective isoforms of MAO, MAO-A and MAO-B, and does so almost equally, with slight preference for the former. By inhibiting MAO, phenelzine prevents the breakdown of the monoamine neurotransmitters serotonin, melatonin, norepinephrine, epinephrine, and dopamine, as well as the trace amine neuromodulators such as phenethylamine, tyramine, octopamine, and tryptamine. This leads to an increase in the extracellular concentrations of these neurochemicals and therefore an alteration in neurochemistry and neurotransmission. This action is thought to be the primary mediator in phenelzine's therapeutic benefits. Phenelzine and its metabolites also inhibit at least two other enzymes to a lesser extent, of which are alanine transaminase (ALA-T),[21] and γ-Aminobutyric acid transaminase (GABA-T),[22] the latter of which is not caused by phenelzine itself, but by a phenelzine metabolite ...
Penemuan penislin selalu dikaitkan dengan ilmuwan Skotlandia, Alexander Fleming pada 1929, walaupun sebenarnya banyak ilmuwan lain yang telah mencatat efek antibakteri sebelum Fleming.[2]. Fleming, dalam laboratoriumnya di Rumah Sakit Santa Maria (kini merupakan salah satu rumah sakit pendidikan di London), mencatat adanya lingkaran hambatan (zona bening) pada pertumbuhan bakteri di piringan kultur Staphylococcus. Fleming menyimpulkan bahwa hambatan itu dikarenakan sebuah subtansi penghambat pertumbuhan dan menghancurkan bakteri. Ia kemudian menumbuhkan sebuah kultur murni dan menemukan Penicillium yang kemudian dikenal sebagai Penicillium chrysogenum. Fleming memberikan istilah "penisilin" untuk menggambarkan hasil filtrasi dari kultur mikrobiologis Penicillium.[2]. Walaupun di tahapan awal ini, penisilin ditemukan efektif melawan bakteri Gram positif dan tidak efektif pada Gram negatif dan jamur. Fleming optimis bahwa penisilin akan menjadi disinfektan yang sangat berguna, berpotensi tinggi ...