Effects of hexamethonium and methyl-p-tyrosine on normal rats subjected to convulsions induced by oxygen at high pressure

1980 ◽  
Vol 58 (3) ◽  
pp. 237-242 ◽  
Author(s):  
E. W. Banister ◽  
A. K. Singh
Keyword(s):  
Amino Acids ◽  
High Pressure ◽  
Protective Action ◽  
Latency Period ◽  
Oxygen Toxicity ◽  
Aminobutyric Acid ◽  
Brain Catecholamines ◽  
Oxidative Deamination ◽  
The Brain ◽  
Catecholamine Concentration

Hexamethonium infusion (intravenous) does not alter the concentrations of brain catecholamines, ammonia, and amino acids in rats under normal conditions. However, it decreases the concentration of blood adrenaline (A) and nonadrenaline (NA) significantly without affecting blood ammonia and amino acids. Injection of α-methyl-p-tyrosine (α-MPT) (intraperitoneal) decreases brain catecholamines without affecting the concentration of ammonia and amino acids in the brain or catecholamines, ammonia, and amino acids in the blood.In normal, hexamethonium-, and α-MFT-treated rats convulsed by exposure to oxygen at high pressure (OHP), the concentration of ammonia and glutamine plus aspargine increased and glutamate and γ-aminobutyric acid (GABA) (brain only) decreased significantly in both blood and brain. After convulsion, hexamethonium and α-MPT effect the same degree of concentration change for ammonia and amino acids in both blood and brain.When hexamethonium-treated rats are convulsed by OHP, the concentrations of A and NA in blood increased significantly. However, the postconvulsive concentration of A in these rats is significantly less than the preconvulsive control values of normal, undrugged rats. Hexamethonium also prolongs the latency period before convulsions induced by exposure of rats to OHP. This protective action of hexamethonium against oxygen toxicity is probably due to (a) some direct effect of low circulating catecholamines, or (b) delay in the production of toxic levels of ammonia from oxidative deamination of catecholamines, as initial low catecholamine concentration would hinder accumulation of ammonia from such deamination.α-MPT treatment was ineffective in producing an increased latency period before convulsion occurred despite the prevailing low brain catecholamine initially produced by α-MPT treatment. However, the concentration of brain A, NA, and total catecholamines decreased significantly after α-MPT-treated rats were convulsed by OHP exposure. The response of blood catecholamines to OHP-induced convulsions in these α-MPT-treated rats is the same as in normal rats.As α-MPT blocks the synthesis of catecholamines, a further decrease in brain catecholamine values after oxygen-induced convulsions in drugged animals suggests that brain catecholamines are oxidatively deaminated to produce ammonia. These observations suggest that, contrary to earlier reports, brain catecholamines do play an important role in producing ammonia during oxygen toxicity, which, in turn, induces convulsions.

The time course of brain and blood catecholamines, catechol O-methyltransferase, and amino acids in rats convulsed by oxygen at high pressure

1979 ◽  
Vol 57 (4) ◽  
pp. 390-395 ◽  
Author(s):  
E. W. Banister ◽  
A. K. Singh
Keyword(s):  
Amino Acids ◽  
High Pressure ◽  
Time Course ◽  
Ammonia Concentration ◽  
Aminobutyric Acid ◽  
Brain Catecholamines ◽  
Oxygen Breathing ◽  
Pressure Oxygen ◽  
High Pressure Oxygen ◽  
Catecholamine Concentration

The time course of changes in blood and brain catecholamines, catechol (O-methyltransferase (COMT), ammonia, and amino acids leading to convulsion by high pressure oxygen breathing (OHP) in rats has been investigated. Brain catecholamines were suppressed by OHP. They changed in phase with brain COMT concentration and consequently were not due to the action of this degrading enzyme. Convulsive actions seem not to be influenced by brain catecholamine concentration. Blood adrenaline concentrations are, however, significantly elevated both prior to and during convulsions. In both brain and blood, ammonia concentration increases, glutamate decreases, and glutamine–aspargine increases. It is proposed that the efficacy of the glutamate–glutamine ammonia buffering system in blood and brain is important in the prevention of the onset of convulsions but that when brain γ-aminobutyric acid is depressed to critical levels, convulsions result.

DELAY OR INHIBITION OF CONVULSIONS BY INTRAPERITONEAL INJECTIONS OF DIVERSE SUBSTANCES

1967 ◽  
Vol 45 (5) ◽  
pp. 857-865 ◽  
Author(s):  
F. V. DeFeudis ◽  
K. A. C. Elliott
Keyword(s):  
Amino Acids ◽  
High Pressure ◽  
Sodium Chloride ◽  
Chloride Solution ◽  
Sodium Chloride Solution ◽  
Strong Solutions ◽  
Aminobutyric Acid ◽  
Plain Water ◽  
Effective Protection ◽  
The Brain

Prior intraperitoneal injections, into mice or rats, of strong solutions of γ-aminobutyric acid, DL-alanine, other amino acids, succinate, or sucrose tend to postpone or prevent convulsions and death caused by the administration of oxygen at high pressure, picrotoxin, or pentylenetetrazol. Sodium chloride solution was not as consistently effective. Protection against strychnine was not obvious. Injections of urea solutions or plain water were not effective. Intraperitoneal injections of the "protective" solutions cause increased osmolarity of the serum and dehydration of the brain; the latter effect may be partly responsible for the elevation of seizure thresholds.

Effect of adrenalectomy on convulsions induced by high-pressure oxygen

1979 ◽  
Vol 57 (7) ◽  
pp. 688-694 ◽  
Author(s):  
A. K. Singh ◽  
E. W. Banister
Keyword(s):  
High Pressure ◽  
Acid Level ◽  
Amino Acid Level ◽  
Aminobutyric Acid ◽  
Pressure Oxygen ◽  
Significant Difference ◽  
High Pressure Oxygen ◽  
Brain Gaba ◽  
The Brain ◽  
Adrenalectomized Rats

Adrenalectomized rats exposed to high pressure oxygen (OHP) until convulsion convulse much later than sham-operated or normal rats. No significant changes in the concentration of noradrenaline (NA) and total catecholamines (TC) in the brain were noted in sham-operated or adrenalectomized rats resulting from sham or real surgery and no change occurred in these variables in normal sham-operated or adrenalectomized animals after OHP leading to convulsion. Brain adrenaline (A) concentration, however, decreased significantly in all three groups following OHP-induced convulsions. Activity of catecholamine O-methyltransferase (COMT) decreased significantly only in adrenalectomized rats. Brain γ-aminobutyric acid (GABA), glutamate, and other amino acid level remained unchanged after adrenalectomy whereas the concentration of ammonia decreased significantly when normal rats were adrenalectomized. After OHP-induced convulsions, the concentrations of brain GABA and glutamate decreased and ammonia and glutamine plus asparagine increased significantly in normal, sham-operated, and adrenalectomized rats. In the blood no significant difference was noted in the concentration of the catecholamines, ammonia, and amino acids either in normal or sham-operated rats. In adrenalectomized rats, the blood A and NA concentrations decreased significantly and tyrosine increased significantly. The concentration of NA, ammonia, and glutamine plus asparagine in rats from all three groups increased after OHP-induced convulsions, whereas the concentration of glutamate decreased significantly. Since the concentration of A increased significantly after convulsions in normal and sham-operated rats but did not change in adrenalectomized rats, it might be proposed that adrenalectomy protects against OHP-induced convulsions by reducing the circulating concentration of A and ammonia.However, these are not the only factors involved in the protection since the sham-operated rats also convulsed much later than normal rats but had similar ammonia and A concentrations to normal animals.

Convulsions and the γ-aminobutyric acid content of rat brain

1968 ◽  
Vol 46 (5) ◽  
pp. 803-804 ◽  
Author(s):  
F. V. DeFeudis ◽  
K. A. C. Elliott
Keyword(s):  
High Pressure ◽  
Rat Brain ◽  
Acid Content ◽  
Aminobutyric Acid ◽  
The Brain

The observation of Wood and Watson that the γ-aminobutyric acid content of the brain decreases in animals that suffer convulsions during treatment with oxygen at high pressure has been confirmed. This decrease is prevented when seizures are prevented by prior intraperitoneal injections of hyperosmotic solutions. When seizures are induced by picrotoxin or pentylenetetrazol the GABA levels are slightly (and alanine levels considerably) increased.

scholarly journals Protective Action of γ-Aminobutyric Acid against Oxygen Toxicity

Nature ◽  
1962 ◽  
Vol 195 (4838) ◽  
pp. 296-296 ◽  
Author(s):  
J. D. WOOD ◽  
W. J. WATSON
Keyword(s):  
Protective Action ◽  
Oxygen Toxicity ◽  
Aminobutyric Acid

The Anticonvulsant Properties of Isonicotinic Acid Hydrazide and Associated Changes in γ-Aminobutyric Acid Metabolism

1973 ◽  
Vol 51 (12) ◽  
pp. 959-965 ◽  
Author(s):  
J. D. Wood ◽  
S. J. Peesker
Keyword(s):  
High Pressure ◽  
Acid Metabolism ◽  
Isonicotinic Acid ◽  
Acid Hydrazide ◽  
Aminobutyric Acid ◽  
Isonicotinic Acid Hydrazide ◽  
Acid Decarboxylase ◽  
Anticonvulsant Action ◽  
Drug Mixture ◽  
The Brain

The administration of isonicotinic acid hydrazide and pyridoxine to chicks prior to their being exposed to oxygen at high pressure brought about a delay in the onset of the hyperbaric-oxygen-induced seizures in the birds. The hydrazide was the active anticonvulsant component of the drug mixture but pyridoxine was necessary to prevent seizures induced by the hydrazide itself shortly after its administration. The anticonvulsant action of the drug mixture developed relatively slowly but lasted for several hours and correlated well with concomitant changes in the concentration of γ-aminobutyric acid (GABA) in the brain. No similar correlation was observed between the anticonvulsant action and the activity of either glutamic acid decarboxylase or GABA-α-oxoglutarate aminotransferase.

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 Ferrier lecture, 1983 - Amino acids and peptides: fast and slow chemical signals in the nervous system?

1984 ◽  
Vol 221 (1224) ◽  
pp. 245-260 ◽  
Keyword(s):  
Amino Acids ◽  
Time Course ◽  
Chemical Signals ◽  
Aminobutyric Acid ◽  
Monoamine Neurotransmitters ◽  
Excitatory Neurotransmitters ◽  
Synaptic Neurotransmission ◽  
Point To Point ◽  
The Brain ◽  
Great Complexity

The classical monoamine neurotransmitters, acetylcholine and the catecholamines, are used by only a small proportion of synapses in mammalian c.n.s. The amino acids GABA (y-aminobutyric acid) and L-glutamate may be the principal inhibitory and excitatory neurotransmitters used for fast point-to-point transmission in the c.n.s. The monoamines and the large number of neuropeptides (over 30) now known to exist in c.n.s. may be chemical signals used for a different type of chemically addressed form of information transmission between neurons in c.n.s. characterized by less precise spatial connections, a slower time course and a far richer diversity of chemical signals than used in classical synaptic neurotransmission. In this context the brain can be viewed as a neuroendocrine secretory organ of great complexity.

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.

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