Effects of 6-hydroxydopamine on brain and blood catecholamines, ammonia, and amino acids in rats

1978 ◽  
Vol 56 (2) ◽  
pp. 331-333 ◽  
Author(s):  
A. K. Singh ◽  
E. W. Banister
Keyword(s):  
Amino Acids ◽  
Adenine Nucleotide ◽  
Aminobutyric Acid ◽  
Nerve Terminals ◽  
Brain Monoamines ◽  
General Stress Response ◽  
Sympathetic Response ◽  
Blood Constituents ◽  
The Central Nervous System ◽  
6 Hydroxydopamine

The effect of 6-hydroxydopamine (6-OHDA) upon brain and blood catecholamines, ammonia, and amino acids has been studied in rats subjected to increasing doses of the drug. Time dependent effects after injection have also been studied. Systemically injected 6-OHDA significantly, acutely reduced brain adrenaline (A), noradrenaline (NA), total catecholamines (TC), γ-aminobutyric acid (GABA), and glutamic acid (Glu); concomitantly brain ammonia (NH3) increased. In blood, NA and TC were reduced and A and NH3 increased. The changes in brain monoamines are surprising since it has been reported that 6-OHDA does not cross the blood-brain barrier. We have proposed that these changes result from a general stress response or a reflex peripheral sympathetic response to falling blood pressure which in some manner communicates to the central nervous system. As the dose of 6-OHDA increased, brain NH3 increased and Glu decreased. A similar effect was seen from a single dose as the time after injection for sampling brain and blood constituents increased. Blood ammonia increases without change in Glu, glutamine, or asparagine. The source of NH3 may be from deamination of adenine nucleotide or catechols released from nerve terminals under the abnormal stimulus of 6-OHDA.

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).

scholarly journals Redistribution of Neuroactive Amino Acids in Hippocampus and Striatum during Hypoglycemia: A Quantitative Immunogold Study

2001 ◽  
Vol 21 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Vidar Gundersen ◽  
Frode Fonnum ◽  
Ole Petter Ottersen ◽  
Jon Storm-Mathisen
Keyword(s):  
Amino Acids ◽  
Glial Cells ◽  
Pyramidal Cell ◽  
Neuronal Death ◽  
Synaptic Vesicles ◽  
Brain Regions ◽  
Aminobutyric Acid ◽  
Nerve Terminals ◽  
Gamma Aminobutyric Acid ◽  
Energy Substrates

Postembedding immunocytochemistry was used to localize aspartate, glutamate, gamma-aminobutyric acid (GABA), and glutamine in hippocampus and striatum during normo- and hypoglycemia in rat. In both brain regions, hypoglycemia caused aspartatelike immunoreactivity to increase. In hippocampus, this increase was evident particularly in the terminals of known excitatory afferents—in GABA-ergic neurons and myelinated axons. Aspartate was enriched along with glutamate in nerve terminals forming asymmetric synapses on spines and with GABA in terminals forming symmetric synapses on granule and pyramidal cell bodies. In both types of terminal, aspartate was associated with clusters of synaptic vesicles. Glutamate and glutamine immunolabeling were markedly reduced in all tissue elements in both brain regions, but less in the terminals than in the dendrosomatic compartments of excitatory neurons. In glial cells, glutamine labeling showed only slight attenuation. The level of GABA immunolabeling did not change significantly during hypoglycemia. The results support the view that glutamate and glutamine are used as energy substrates in hypoglycemia. Under these conditions both excitatory and inhibitory terminals are enriched with aspartate, which may be released from these nerve endings and thus contribute to the pattern of neuronal death characteristic of hypoglycemia.

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.

Free Amino Acids in Cytosol of Rat Brain after Intraventricular Administration of 5,6-Dihydroxytryptamine and 6-Hydroxydopamine

1987 ◽  
Vol 42 (5) ◽  
pp. 637-640
Author(s):  
Janusz Konecki ◽  
Janusz Gabrys ◽  
Ryszard Brus ◽  
Ryszard Szkilnik ◽  
Jashovam Shani
Keyword(s):  
Amino Acids ◽  
Free Amino Acids ◽  
Free Amino ◽  
Brain Structures ◽  
Aminobutyric Acid ◽  
Intraventricular Administration ◽  
Gamma Aminobutyric Acid ◽  
Male Wistar Rats ◽  
6 Hydroxydopamine ◽  
The Brain

Abstract Levels of 24 free amino acids were estimated in the brain after administration of 5,6-dihydroxy-tryptamine and 6-hydroxydopamine into the lateral brain ventricles of male Wistar rats. These neurotransmitters caused serotoninectomy and sympathectomy in the diencephalon, striatum, brain stem and medulla, thalamus and hypothalamus, cerebral cortex and cerebellum. The most abundant amino acids in these brain structures were: glutamic acid, serine, aspartic acid, cystine, gamma-aminobutyric acid, glycine, tryptophan and alanine. We detected and quantified changes in the levels of these and other amino acids in the investigated regions of the rat central nervous system, under the influence of these two neurotransmitters.

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.

PROTECTIVE EFFECT OF POLYPEPTIDE AND AMINO ACIDS ON THE DEVELOPMENT OF THE NERVOUS TISSUE CULTURE IN THE PRESENCE OF CYCLOPHOSPHAMIDE

2017 ◽  
pp. 22-26
Author(s):  
V. B. Dolgo-Saburov ◽  
N. I. Chalisova ◽  
L. V. Lyanginen ◽  
E. S. Zalomaeva
Keyword(s):  
Amino Acids ◽  
Cell Proliferation ◽  
Tissue Culture ◽  
Protective Effect ◽  
Organotypic Culture ◽  
Inhibitory Effect ◽  
Mustard Gas ◽  
Synthesis Inhibitor ◽  
Combined Administration ◽  
The Central Nervous System

In an organotypic culture, an investigation was conducted into combined effects of cyclophosphamide DNA as synthesis inhibitor used to model a resorptive action of mustard gas, and cortexin polypeptide or each of 20 encoded amino acids on the development of cell proliferation in cerebral cortex explants of the rat. The combined administration of cyclophosphamide together with cortexin or with each of the 20 encoded amino acids, except glycine, showed suppression of the cytostatic agent inhibitory effect. Thus, cortexin and amino acids have a protective effect on cell proliferation in the tissue culture of the central nervous system under the action of mustardlike substances.

A radiotracer method for the measurement of central nervous system catecholamines in vivo

1978 ◽  
Vol 56 (3) ◽  
pp. 535-538 ◽  
Author(s):  
S. W. Tang ◽  
H. C. Stancer ◽  
J. J. Warsh
Keyword(s):  
Central Nervous System ◽  
Animal Model ◽  
Nervous System ◽  
Specific Activity ◽  
Brain Catecholamines ◽  
Radiotracer Method ◽  
New Strategy ◽  
The Central Nervous System ◽  
6 Hydroxydopamine

A new strategy for measurement of brain catecholamines was tested in an animal model. [3H]Norepinephrine was infused intravenously in rabbits to label the peripheral norepinephrine pools. The specific activity of urinary 3-methoxy-4-hydroxymandelic acid was consistently higher than that for 3-methoxy-4-hydroxyphenylglycol (MHPG). Central sympathectomy with 6-hydroxydopamine abolished this difference. Using the formula we propose, it is estimated that 30–50% of urinary MHPG originates from the central nervous system.

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