GABA Accumulation

Researchers have reported that under anaerobic conditions, the oxidation of phosphoric acid in the mitochondria of plants became weakened and reduction potential increased. That means the ratio of NADH and NAD-r increased and ADP transformed to ATP. This caused the dehydrogenation activity of succinic semialdehyde dehydrogenase to decrease, and resulted in weakening the reaction of succinic semialdehyde dehydrogenase to form succinate this is beneficial to the accumulation of GABA in tea leaves. Sawai et al. further reported that the amount of 

During tea mannfacture, the plucked fresh tea leaves are first subjected to withering. The water permeability of the cell wall and membrane increases as the tea leaves keep losing water with concurrent increase of hydrolysis activity. The amount of theanine and glntamine is reduced due to hydrolysis, so that the amount of glutamate is greatly increased and the GAD activity is induced. Therefore, further anaerobic treatment resnlts in the accumulation of GABA in tea leaves.  

The optimal pH values for GAD and GABA-transaminase activities are around 5.8 and 8.9. Dnring withering (a kind of stress), the pH of cell cytoplast in tea leaves was decreased. Therefore, it favored the GAD but not GABA-transaminase activity. It resnlted in the block of GABA transamination and further GABA accumulation. 

Damaging of the cell membrane may cause increased formation of GABA. Therefore, nsing machinery force to damage the cell membrane is a good and effective way to produce GABA. 

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Redburn DA, Madtes P Jr. 1986. Postnatal development of 3H-GABA-accumulating cells in rabbit retina. J Comp Neurol 243 41-57. 

The cellular localization of a sodium-dependent GABA uptake system has been described in A. suum (149). [ H]GABA accumulates in muscle cells and a small subset of neurons. These neurons show only partial overlap with the neurons that express GABA. The dorsal and ventral inhibitory motoneurons show intense GABA staining. 

Ozkan ED, Lee FS, Ueda T. A protein factor that inhibits ATP-dependent glutamate and GABA accumulation into synaptic vesicles purification and initial characterization. Proc Natl Acad Sci USA 1997 94 4137-4142. 

Hampton C K and Redburn D, A (1983) Autoradiographic analysis of H-glutamate, H-dopamine and H-GABA accumulation m rabbit retina after kamic acid treatment. /. Neurosci. Res 9, 239-251... 

Perez de la Mora M, Fuxe K, Hokfelt T, and Ljungdahl A (1977) Evidence for an impulse-dependent GABA accumulation in the substantia nigra after treatment with y-glutamyl-hydrazide Neurosci Lett 5, 75-82... 

The exocytotic release of neurotransmitters from synaptic vesicles underlies most information processing by the brain. Since classical neurotransmitters including monoamines, acetylcholine, GABA, and glutamate are synthesized in the cytoplasm, a mechanism is required for their accumulation in synaptic vesicles. Vesicular transporters are multitransmembrane domain proteins that mediate this process by coupling the movement of neurotransmitters to the proton electrochemical gradient across the vesicle membrane. 

All cell membranes contain transmembrane proteins that form ion channels. These ion channels are usually selectively permeable to particular ions. Some channels, such as GABA-gated ion channels, are permeable to Cl ions and are inhibitory in nature because they make the inside of the nerve or muscle cells more negative as the Cl ions enter. Some ion channels are permeable to the cations Na and K, and an example of this type is the nicotinic acetylcholine-gated channel. Nicotinic channels have an excitatory effect when they open because Na ions enter and K ions leave through these channels. The cell becomes more positive inside and depolarizes. If the cell is a muscle cell, calcium accumulates in the cytoplasm and it contracts. We have found that all over the surface of Ascaris muscle there are GABA receptors (Martin, 1980) as well as nicotinic acetylcholine channels (Martin, 1982 Robertson and Martin, 1993). 

The answer is c. (Hardman, p 481. Katzung, pp 404-405.) Vigabatrin is useful in partial seizures. It is an irreversible inhibitor of GABA aminotransferase, an enzyme responsible for the termination of GABA action. This results in accumulation of GABA at synaptic sites, thereby enhancing its effect. 

In the past decade, considerable evidence has accumulated that a primary molecular target of general anesthetics is the GABA receptor-chloride channel, a major mediator of inhibitory synaptic transmission. Inhaled anesthetics,... 

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