scholarly journals Effect of excitatory amino acids on gamma-aminobutyric acid release from frog horizontal cells.

1985 ◽  
Vol 362 (1) ◽  
pp. 51-67 ◽  
Author(s):  
J R Cunningham ◽  
M J Neal
Keyword(s):  
Amino Acids ◽  
Excitatory Amino Acids ◽  
Horizontal Cells ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Acid Release

scholarly journals Glutamate and psychiatric disorders

2002 ◽  
Vol 8 (3) ◽  
pp. 189-197 ◽  
Author(s):  
Eva M. Tsapakis ◽  
Michael J. Travis
Keyword(s):  
Amino Acids ◽  
Central Nervous System ◽  
Excitatory Amino Acids ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Neuronal Inhibition ◽  
The Central Nervous System ◽  
Excitatory Neurotransmission ◽  
Almost All ◽  
Glutamate System

Most of the excitatory neurotransmission in the central nervous system (CNS) is mediated by the endogenous excitatory amino acids (EAAs) glutamate, aspartate and homocysteine. Most of the endogenous inhibitory neurotransmission is mediated by gamma-aminobutyric acid (GABA). EAAs modulate the firing of almost all neurons in the CNS, as excitatory neurotransmission can result in both neuronal inhibition and excitation. The glutamate system is the best characterised of the EAA systems (Box 1).

Effects of Hypothermia, Pentobarbital, and Isoflurane on Postdepolarization Amino Acid Release during Complete Global Cerebral Ischemia

1996 ◽  
Vol 85 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Ken Nakashima ◽  
Michael M. Todd
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Cerebral Ischemia ◽  
Excitatory Amino Acids ◽  
High Performance ◽  
Excitatory Amino Acid ◽  
Protective Efficacy ◽  
Aminobutyric Acid ◽  
Global Cerebral Ischemia ◽  
Gamma Aminobutyric Acid

Background Hypothermia and anesthetics may protect the brain during ischemia by blocking the release of excitatory amino acids. The effects of hypothermia (28 degrees C), pentobarbital, and isoflurane on postischemic excitatory amino acid concentrations were compared. Methods Rats were anesthetized with 0.8% halothane/50% N2O, vascular catheters were placed, and a glass microelectrode and microdialysis cannula were inserted into the cerebral cortex. Experimental groups were: (1) control, pericranial, t = 38 degrees C; (2) hypothermia, t = 28 degrees C; (3) pentobarbital, t = 38 degrees C; and (4) isoflurane, t = 38 degrees C. Halothane/N2O was continued in groups 1 and 2, whereas a deep burst-suppression or isoelectric electroencephalogram was achieved with the test drugs in groups 3 and 4. Cerebral metabolic rates were similar in groups 2, 3, and 4. After a baseline dialysis sample was collected, animals were killed with potassium chloride. The time to terminal depolarization was recorded, after which three consecutive 10-min dialysate samples were collected. Glutamate, aspartate, gamma-aminobutyric acid, and glycine concentrations were measured using high-performance liquid chromatography. Results Times to terminal depolarization were shorter in both pentobarbital and isoflurane groups than with hypothermia (103 +/- 15 and 127 +/- 10 vs. 195 +/- 20 s respectively, mean +/- SD). However, times to terminal depolarization in all three groups were longer than in control subjects (control = 70 +/- 9s). Postdepolarization concentrations of all compounds were lower in hypothermic animals (vs. normothermic control animals), but no reductions in glutamate, aspartate, or glycine concentrations were noted in pentobarbital or isoflurane groups. gamma-Aminobutyric acid concentrations were reduced by both anesthetics, but not to the same degree as with hypothermia. Conclusions Pentobarbital and isoflurane prolonged the time to terminal depolarization, but did not influence the rate at which the extracellular concentrations of glutamate, aspartate, or glycine increased. By contrast, hypothermia reduced the release of all excitatory amino acids. These differences may explain the greater protective efficacy of hypothermia in the face of cerebral ischemia.

Baclofen: effects on amino acid release

1978 ◽  
Vol 56 (1) ◽  
pp. 150-154 ◽  
Author(s):  
S. J. Potashner
Keyword(s):  
Amino Acids ◽  
Excitatory Amino Acids ◽  
The Other ◽  
Aminobutyric Acid ◽  
Nerve Terminals ◽  
Amino Butyric Acid ◽  
Acid Release ◽  
Afferent Terminals ◽  
Excitatory Transmitter ◽  
Stimulation Of

This study investigated the effects of the antispastic drug β-(p-chlorophenyl)-γ-amino-butyric acid (Baclofen) on the release of amino acids from slices of guinea pig cerebral cortex. Electrical stimulation of slices evoked the release of endogenous14C-labelled glutamate, aspartate, γ-aminobutyric acid (GABA), alanine, and threonine–serine–glutamine (labelled via metabolism of D-[U-14C]glucose), and of exogenous glutamate, aspartate, GABA, and α-aminoisobutyrate. The releases of endogenous14C-labelled glutamate, aspartate, and GABA were three to seven times larger than those of other amino acids. Baclofen (4 μM) inhibited the evoked release of endogenous 14C-labelled glutamate and aspartate by nearly 60%, that of endogenous14C-labelled threonine–serine–glutamine and alanine by 14–19%, but had no effect on that of endogenous14C-labelled GABA. The drug inhibited the evoked release of the exogenous amino acids by 25–32%. Baclofen doubled the incorporation of 14C from D-[U-14C]glucose into endogenous alanine but was without effect on either the incorporation of 14C into the other endogenous amino acids or the turnover of any of the endogenous14C-labelled amino acids. Because endogenous14C-labelled glutamate, aspartate, and GABA are probably released from nerve terminals, Baclofen selectively suppresses the release of excitatory amino acids from nerve terminals. Similarly, depression of the release of excitatory transmitter (presumably glutamate) from primary afferent terminals in the spinal cord may at least partly explain the antispastic action of Baclofen.

Purification of Antihemophilic Factor (Factor VIII) by Amino Acid Precipitation*

1964 ◽  
Vol 11 (01) ◽  
pp. 064-074 ◽  
Author(s):  
Robert H Wagner ◽  
William D McLester ◽  
Marion Smith ◽  
K. M Brinkhous
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Factor Viii ◽  
Plasma Protein ◽  
Acid Precipitation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Specific Procedure ◽  
Beta Alanine ◽  
Antihemophilic Factor

Summary1. The use of several amino acids, glycine, alpha-aminobutyric acid, alanine, beta-alanine, and gamma-aminobutyric acid, as plasma protein precipitants is described.2. A specific procedure is detailed for the preparation of canine antihemophilic factor (AHF, Factor VIII) in which glycine, beta-alanine, and gammaaminobutyric acid serve as the protein precipitants.3. Preliminary results are reported for the precipitation of bovine and human AHF with amino acids.

scholarly journals Inositol incorporation into phosphoinositides in retinal horizontal cells of Xenopus laevis: enhancement by acetylcholine, inhibition by glycine.

1984 ◽  
Vol 99 (2) ◽  
pp. 686-691 ◽  
Author(s):  
R E Anderson ◽  
J G Hollyfield
Keyword(s):  
Xenopus Laevis ◽  
Culture Medium ◽  
Photoreceptor Cells ◽  
Horizontal Cells ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Light Effect ◽  
Synaptic Inputs ◽  
Absorption Of Light

The absorption of light by photoreceptor cells leads to an increased incorporation of [2-3H]inositol into phosphoinositides of horizontal cells in the retina of Xenopus laevis in vitro. We have identified several retinal neurotransmitters that are involved in regulating this response. Incubation with glycine, the neurotransmitter of an interplexiform cell that has direct synaptic input onto horizontal cells, abolishes the light effect. This inhibition is reversed by preincubation with strychnine. Acetylcholine added to the culture medium enhances the incorporation of [2-3H]inositol into phosphoinositides in horizontal cells when retinas are incubated in the dark. This effect is inhibited by preincubation with atropine. However, atropine alone does not inhibit the light-enhanced incorporation of [2-3H]inositol into phosphoinositides in the retina. gamma-Aminobutyric acid, the neurotransmitter of retinal horizontal cells in X. laevis, as well as dopamine and norepinephrine, have no effect on the incorporation of [2-3H]inositol into phosphoinositides. These studies demonstrate that the light-enhanced incorporation of [2-3H]inositol into phosphoinositides of retinal horizontal cells is regulated by specific neurotransmitters, and that there are probably several synaptic inputs into horizontal cells which control this process.

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