scholarly journals Putrescine, a source of γ-aminobutyric acid in the adrenal gland of the rat

1988 ◽  
Vol 251 (2) ◽  
pp. 559-562 ◽  
Author(s):  
P C Caron ◽  
L J Cote ◽  
L T Kremzner
Keyword(s):  
Adrenal Gland ◽  
Diamine Oxidase ◽  
Cell Metabolism ◽  
Turnover Time ◽  
Oxidase Inhibitor ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba Concentration ◽  
The Brain

Putrescine is the major source of gamma-aminobutyric acid (GABA) in the rat adrenal gland. Diamine oxidase, and not monoamine oxidase, is essential for GABA formation from putrescine in the adrenal gland. Aminoguanidine, a diamine oxidase inhibitor, decreases the GABA concentration in the adrenal gland by more than 70% after 4 h, and almost to zero in 24 h. Studies using [14C]putrescine confirm that [14C]GABA is the major metabolite of putrescine in the adrenal gland. Inhibition of GABA transaminase by amino-oxyacetic acid does not change the GABA concentration in the adrenal gland, as compared with the brain, where the GABA concentration rises. With aminoguanidine, the turnover time of GABA originating from putrescine in the adrenal gland is 5.6 h, reflecting a slower rate of GABA metabolism compared with the brain. Since GABA in the adrenal gland is almost exclusively derived from putrescine, the role of GABA may relate to the role of putrescine as a growth factor and regulator of cell metabolism.

GAMMA-AMINOBUTYRIC ACID LEVELS IN THE BRAIN OF RATS EXPOSED TO OXYGEN AT HIGH PRESSURES

1963 ◽  
Vol 41 (9) ◽  
pp. 1907-1913 ◽  
Author(s):  
J. D. Wood ◽  
W. J. Watson
Keyword(s):  
High Pressure ◽  
Recovery Time ◽  
High Pressures ◽  
No Reduction ◽  
Ambient Pressure ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba Concentration ◽  
Short Period ◽  
The Brain

Rats were exposed to 100% oxygen at a pressure of 6 atmospheres absolute for 33 minutes. The surviving animals were assigned to one of three groups: (a) animals suffering severe convulsions during exposure, (b) animals suffering mild convulsions during exposure, (c) animals in which no convulsions were observed during exposure. The concentration of gamma-aminobutyric acid (GABA) in the brains of rats in all groups was lower than in unexposed rats, reductions of 35%, 27%, and 19% in GABA concentration being observed in groups (a), (b), and (c) respectively. Only a few minutes' exposure to oxygen at high pressure was necessary to cause a significant decrease in GABA concentration. Exposure either to air at high pressure or to 100% oxygen at ambient pressure produced no reduction in GABA levels. Although the GABA concentration in the brain increased markedly within 1 hour after the end of the 33-minute exposure to oxygen at 6 atm pressure it was still somewhat below the levels found in unexposed animals. No significant change in GABA levels was observed during a further 2 hours of recovery time. In the case of rats exposed for only a short period of time, however, a complete return to normal was observed within the first hour. The levels of glutamic acid, aspartic acid, and total α-amino acids in the brain were not altered by exposure to oxygen at high pressure.

The GABA system and addiction

2018 ◽  
Author(s):  
David J. Nutt ◽  
Liam J. Nestor
Keyword(s):  
Potential Role ◽  
Abuse Liability ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Substance Addiction ◽  
Inhibitory Neurotransmitter ◽  
Gaba System ◽  
Clinical Potential ◽  
The Brain

Research points to the potential role of gamma-aminobutyric acid (GABA) in substance addiction. GABA is the major inhibitory neurotransmitter in the brain. Disturbances in the GABA system may predate substance abuse and addiction, whereby its efficacy to modulate other neurotransmitter systems (e.g. dopamine) strongly implicated in substance addiction behaviours is impaired. There are a number of addictive substances that boost GABA functioning, however, such as alcohol and benzodiazepines. Medications that boost the availability of GABA or mimic its effects at receptors may possess some clinical potential in treating addiction, but also have abuse liability.

GAMMA-AMINOBUTYRIC ACID LEVELS IN THE BRAIN OF RATS EXPOSED TO OXYGEN AT HIGH PRESSURES

1963 ◽  
Vol 41 (1) ◽  
pp. 1907-1913 ◽  
Author(s):  
J. D. Wood ◽  
W. J. Watson
Keyword(s):  
High Pressure ◽  
Recovery Time ◽  
High Pressures ◽  
No Reduction ◽  
Ambient Pressure ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba Concentration ◽  
Short Period ◽  
The Brain

Rats were exposed to 100% oxygen at a pressure of 6 atmospheres absolute for 33 minutes. The surviving animals were assigned to one of three groups: (a) animals suffering severe convulsions during exposure, (b) animals suffering mild convulsions during exposure, (c) animals in which no convulsions were observed during exposure. The concentration of gamma-aminobutyric acid (GABA) in the brains of rats in all groups was lower than in unexposed rats, reductions of 35%, 27%, and 19% in GABA concentration being observed in groups (a), (b), and (c) respectively. Only a few minutes' exposure to oxygen at high pressure was necessary to cause a significant decrease in GABA concentration. Exposure either to air at high pressure or to 100% oxygen at ambient pressure produced no reduction in GABA levels. Although the GABA concentration in the brain increased markedly within 1 hour after the end of the 33-minute exposure to oxygen at 6 atm pressure it was still somewhat below the levels found in unexposed animals. No significant change in GABA levels was observed during a further 2 hours of recovery time. In the case of rats exposed for only a short period of time, however, a complete return to normal was observed within the first hour. The levels of glutamic acid, aspartic acid, and total α-amino acids in the brain were not altered by exposure to oxygen at high pressure.

Changes in gamma-aminobutyric acid and somatostatin in epileptic cortex associated with low-grade gliomas

1992 ◽  
Vol 77 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Michael M. Haglund ◽  
Mitchel S. Berger ◽  
Dennis D. Kunkel ◽  
JoAnn E. Franck ◽  
Saadi Ghatan ◽  
...  
Keyword(s):  
Epileptiform Activity ◽  
Aminobutyric Acid ◽  
Low Grade ◽  
Tumor Infiltration ◽  
Gamma Aminobutyric Acid ◽  
Content Type ◽  
Low Grade Gliomas ◽  
Neuronal Populations ◽  
Significant Difference

✓ The role of specific neuronal populations in epileptic foci was studied by comparing epileptic and nonepileptic cortex removed from patients with low-grade gliomas. Epileptic and nearby (within 1 to 2 cm) nonepileptic temporal lobe neocortex was identified using electrocorticography. Cortical specimens taken from four patients identified as epileptic and nonepileptic were all void of tumor infiltration. Somatostatin- and γ-aminobutyric acid (GABAergic)-immunoreactive neurons were identified and counted. Although there was no significant difference in the overall cell count, the authors found a significant decrease in both somatostatin- and GABAergic-immunoreactive neurons (74% and 51 %, respectively) in the epileptic cortex compared to that in nonepileptic cortex from the same patient. It is suggested that these findings demonstrate changes in neuronal subpopulations that may account for the onset and propagation of epileptiform activity in patients with low-grade gliomas.

scholarly journals Levels of biogenic amines in the brain of rats at experimental post-traumatic stress disorder development

2015 ◽  
Vol 96 (5) ◽  
pp. 806-810
Author(s):  
R V Deev ◽  
Yu M Shatrova ◽  
A I Sinitskiy ◽  
N S Molchanova ◽  
A K Yunusova ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Acid Level ◽  
Stress Disorder ◽  
Aminobutyric Acid ◽  
Behavioral Activity ◽  
Gamma Aminobutyric Acid ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Brain

Aim. To study the changes in levels of biogenic amines-neurotransmitters in the brain at experimental post-traumatic stress disorder development in rats. Methods. Post-traumatic stress disorder was modeled by keeping 48 outbred male rats in under constant and inescapable strong unconditioned stimulus. The control group included 16 intact animals, not exposed to stress influences. The levels of 3,4-dihydroxyphenylalanine, dopamine, norepinephrine, epinephrine and gamma-aminobutyric acid were determined by fluorometric methods. Behavioral activity of animals was evaluated on the day 3, 7, 10 and 14 by «open field» and «elevated plus maze» actinographs. Results. When comparing the concentrations of studied neurotransmitters in the brain of control animals with experimental groups, reflecting the development of post-traumatic stress disorder at the time, adrenaline and 3,4-dihydroxyphenylalanine levels were increased on the third day, level of norepinephrine was reduced on the seventh day, 3,4-dihydroxyphenylalanine, dopamine, norepinephrine levels were elevaled, gamma-aminobutyric acid level was reduced on the tenth day, gamma-aminobutyric acid level was increased on the fourteenth day after the stress. Conclusion. According to the results of the correlation analysis, the largest contribution to the development of behavioral disorders are made by altered brain level of gamma-aminobutyric acid at the time of post-traumatic stress disorder formation (tenth and fourteenth day). At the earlier stages (third and seventh day), the relationship of rats behavioral activity and altered 3,4-dihydroxyphenylalanine and norepinephrine brain levels was shown.

The Effects of Agonists of Ionotropic GABAAand Metabotropic GABABReceptors on Learning

2009 ◽  
Vol 12 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Evgeniya A. Zyablitseva ◽  
Nikolay S. Kositsyn ◽  
Galina I. Shul'gina
Keyword(s):  
Affect Regulation ◽  
Gaba Receptors ◽  
Conditioned Inhibition ◽  
Early Stage ◽  
Dominant Role ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Internal Inhibition ◽  
Selective Agonist ◽  
The Brain

The research described here investigates the role played by inhibitory processes in the discriminations made by the nervous system of humans and animals between familiar and unfamiliar and significant and nonsignificant events. This research compared the effects of two inhibitory mediators of gamma-aminobutyric acid (GABA): 1) phenibut, a nonselective agonist of ionotropic GABAAand metabotropic GABABreceptors and 2) gaboxadol a selective agonist of ionotropic GABAAreceptors on the process of developing active defensive and inhibitory conditioned reflexes in alert non-immobilized rabbits. It was found that phenibut, but not gaboxadol, accelerates the development of defensive reflexes at an early stage of conditioning. Both phenibut and gaboxadol facilitate the development of conditioned inhibition, but the effect of gaboxadol occurs at later stages of conditioning and is less stable than that of phenibut. The earlier and more stable effects of phenibut, as compared to gaboxadol, on storage in memory of the inhibitory significance of a stimulus may occur because GABABreceptors play the dominant role in the development of internal inhibition during an early stage of conditioning. On the other hand this may occur because the participation of both GABAAand GABABreceptors are essential to the process. We discuss the polyfunctionality of GABA receptors as a function of their structure and the positions of the relevant neurons in the brain as this factor can affect regulation of various types of psychological processes.

Brain amino acid concentrations during diving and acid-base stress in turtles

1985 ◽  
Vol 58 (6) ◽  
pp. 1751-1754 ◽  
Author(s):  
B. M. Hitzig ◽  
M. P. Kneussl ◽  
V. Shih ◽  
R. D. Brandstetter ◽  
H. Kazemi
Keyword(s):  
Amino Acid ◽  
Aminobutyric Acid ◽  
Breath Hold ◽  
Gamma Aminobutyric Acid ◽  
Amino Acid Neurotransmitters ◽  
Acid Base ◽  
Ventilatory Drive ◽  
Amino Acid Concentrations ◽  
Brain Amino Acid

To assess the role of brain amino acid neurotransmitters in the breath hold of diving animals, concentrations of free amino acids present in the brains of turtles immediately after 2 h of apneic diving (at 20 degrees C) were measured. Additionally, the same measurements were performed on four other groups of animals subjected to 2 h of hypercapnia (8% CO2 in air), anoxia (N2 breathing), anoxia plus hypercapnia (8% CO2–92% N2), or air breathing (control). Significant changes in the concentrations of the inhibitory amino acid neurotransmitters known to affect respiration [gamma-aminobutyric acid (GABA) and taurine] were seen. GABA increased significantly in those animals subjected to anoxia, whereas taurine decreased significantly in the diving animals and increased significantly in those subjected to anoxia plus hypercapnia. These results suggest that the attenuated central ventilatory drive during diving in these animals may be related to alterations in brain concentrations of GABA and taurine.

Changes in renal and central noradrenergic activity with potassium in DOCA-salt rats

1984 ◽  
Vol 246 (5) ◽  
pp. F670-F675 ◽  
Author(s):  
T. Fujita ◽  
Y. Sato
Keyword(s):  
Urinary Sodium Excretion ◽  
Turnover Time ◽  
Hypertensive Rats ◽  
Potassium Supplement ◽  
Norepinephrine Concentration ◽  
Norepinephrine Turnover ◽  
Salt Hypertension ◽  
Rate Of Decline ◽  
The Brain

We studied the role of the renal and central noradrenergic neurons in the antihypertensive actions of potassium in DOCA-salt hypertensive rats. Supplementation with 0.2% KCl could moderate the development of the DOCA-salt hypertension. The potassium supplement attenuated sodium retention in the DOCA-salt rats, and, thus, sodium "space" at wk 4 was significantly smaller in the KCl-supplemented DOCA-salt rats than in the DOCA-salt rats. Norepinephrine turnover was measured from the rate of decline of tissue norepinephrine concentration after administration of alpha-methyl-p-tyrosine. Renal norepinephrine turnover was markedly accelerated in the DOCA-salt rats compared with the vehicle-treated control rats, but the 0.2% KCl supplements could normalize it. In contrast, turnover time in the hypothalamus and pons medulla was delayed in the DOCA-salt rats compared with the control rats, whereas 0.2% KCl supplements increased the norepinephrine turnover in the brain stem. These results suggest that the potassium-induced hypotensive actions in DOCA-salt rats may be attributed mainly to the augmented urinary sodium excretion. Moreover, it appears that the normalization of the increased renal sympathetic activity, which is intimately related to the central sympathoinhibitory noradrenergic mechanisms, may be involved in the natriuretic and antihypertensive actions of potassium in DOCA-salt hypertensive rats.

scholarly journals Metabolomic changes in animal models of depression: a systematic analysis

2021 ◽  
Author(s):  
Juncai Pu ◽  
Yiyun Liu ◽  
Siwen Gui ◽  
Lu Tian ◽  
Yue Yu ◽  
...  
Keyword(s):  
Animal Models ◽  
Large Scale ◽  
Hippuric Acid ◽  
Aminobutyric Acid ◽  
Blood Metabolites ◽  
Pimelic Acid ◽  
Gamma Aminobutyric Acid ◽  
Systematic Analysis ◽  
Animal Models Of Depression ◽  
The Brain

AbstractExtensive research has been carried out on the metabolomic changes in animal models of depression; however, there is no general agreement about which metabolites exhibit constant changes. Therefore, the aim of this study was to identify consistently altered metabolites in large-scale metabolomics studies of depression models. We performed vote counting analyses to identify consistently upregulated or downregulated metabolites in the brain, blood, and urine of animal models of depression based on 3743 differential metabolites from 241 animal metabolomics studies. We found that serotonin, dopamine, gamma-aminobutyric acid, norepinephrine, N-acetyl-L-aspartic acid, anandamide, and tryptophan were downregulated in the brain, while kynurenine, myo-inositol, hydroxykynurenine, and the kynurenine to tryptophan ratio were upregulated. Regarding blood metabolites, tryptophan, leucine, tyrosine, valine, trimethylamine N-oxide, proline, oleamide, pyruvic acid, and serotonin were downregulated, while N-acetyl glycoprotein, corticosterone, and glutamine were upregulated. Moreover, citric acid, oxoglutaric acid, proline, tryptophan, creatine, betaine, L-dopa, palmitic acid, and pimelic acid were downregulated, and hippuric acid was upregulated in urine. We also identified consistently altered metabolites in the hippocampus, prefrontal cortex, serum, and plasma. These findings suggested that metabolomic changes in depression models are characterized by decreased neurotransmitter and increased kynurenine metabolite levels in the brain, decreased amino acid and increased corticosterone levels in blood, and imbalanced energy metabolism and microbial metabolites in urine. This study contributes to existing knowledge of metabolomic changes in depression and revealed that the reproducibility of candidate metabolites was inadequate in previous studies.

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