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Biomedical subjects

J Coutinho-Netto

Publications and source records attributed to J Coutinho-Netto.

26 records · Page 2Linked to original sources
PubMed1981

Effect of beta-bungarotoxin on the release of endogenous amino aids from the sensorimotor cortex.

beta-Bungarotoxin, a snake neurotoxin purified from the venom of Bungarus multicinctus, caused a significant increase in the in vivo release of glutamate from the superfused sensorimotor cortex of awake animals. A smaller effect on GABA release was observed, but no change was detected in the release of six other amino acids measured. The effects on glutamate and GABA release were entirely blocked by tetrodotoxin (1 micrometer) and were reversible when the cortical tissue was washed with saline.

Amino Acids↗
PubMed1981

Effect of depolarizing agents on the incorporation of amino acids into soluble cytoplasmic and membrane-bound proteins of synaptosome fractions.

The incorporation of [U-14C] protein hydrolysate and [U-14C]leucine into the trichloroacetic acid (TCA)-insoluble membrane and the soluble synaptoplasm proteins of synaptosomes was studied. Following treatment with the depolarizing agents veratrine, Tityus toxin, or potassium, the specific radioactivity of both precursor pool and proteins were measured to examine the link between protein labeling and the fall in the free amino acid pool due to depolarization-induced release of glutamate and aspartate. By reducing the size of the fall in precursor pool due to depolarization by using a nontransmitter amino acid such as leucine (as compared with the usual use of protein hydrolysate), it was shown that the amount of which the pool is reduced is proportional to the change in the protein labeling observed. These results confirm that membrane depolarization causes a large increase in the labeling of membrane-bound proteins as compared with the soluble synaptosomal proteins.

Amino Acids↗
PubMed1981

Is glutamate a trigger factor in epileptic hyperactivity?

The effects of glutamate and aspartate antagonists were studied on limb-jerk frequency and EEG patterns in rats made epileptic by cobalt implantation in the sensorimotor cerebral cortex. The results of this study were as follows: (1) alpha-Amino-4-phosphonobutyric acid (0.055--1.10 mM) decreased or completely prevented the epileptic manifestations. The effect was reversible 30 min after washing with artificial CSF solution. (2) DL-Pyroglutamic acid completely abolished the myoclonic jerks and EEG spikes. (3) alpha-Amino-5-phosphonovaleric acid and alpha-D-amino-adipic acid significantly reduced the frequency of epileptic spikes and myoclonic jerks. (4) Other analogs, alpha-amino-3-phosphonopropionic acid (0.6 mM), alpha-amino phosphonocaproic acid (0.95), and hydroxy-3-amino pyrrolidone-2 were without effect. (5) Glutamate itself did not decrease the epileptic manifestations.

Amino Acids↗
PubMed1980

The action of gamma-vinyl-GABA and gamma-acetylenic-GABA on the resting and stimulated release of GABA in vivo.

The effects of gamma-vinyl-GABA (4-amino-hex-5-enoic acid, RMI 71754) and gamma-acetylenic-GABA (4-amino-hex-5-ynoic acid, RMI 71645), the selective and irreversible inhibitors of GABA-transaminase (E.C. 2.6.1.19), on the resting and stimulated release of GABA and other amino acids from sensorimotor cortex of rats was studied using a superfusion technique. Administration of a single dose of gamma-vinyl-GABA (1500 mg/kg i.p.) caused the appearance of GABA in superfusate. This reached a maximal peak size after 50 min and remained high for 3 h. gamma-Vinyl-GABA was also released and reached a maximum value after 20 min and decreased to low levels during 3 h. There was no direct parallelism between the time courses of release of GABA and gamma-vinyl-GABA. Also, the amount of GABA released was much larger when the drug was administered by i.p. injection than when applied directly to the cortex surface through the cannula at 100 microM. In the presence of gamma-vinyl-GABA, stimulation of the brachial plexus contralateral to the superfusion cannula increased GABA and glutamate release, but was without effect on gamma-vinyl-GABA itself or any other amino acid. In the presence of gamma-acetylenic-GABA the contralateral stimulation increased significantly only the rate of release of glutamate and the combined peaks of GABA and gamma-acetylenic-GABA. These changes were not observed to follow stimulation of the ipsilateral plexus. Stimulation of either plexus had no detectable action on the rates of release of GABA from the visual cortex. The changes in rates of release of GABA and glutamate due to stimuli were reversible, returning to control levels after cessation of the stimulation.

4-Aminobutyrate Transaminase↗
PubMed1980

The effects of scorpion venom toxin on the release of amino acid neurotransmitters from cerebral cortex in vivo and in vitro.

Tityustoxin, the active component of the venom of the Brazilian yellow scorpion Tityus serrulatus, caused specific release of the neurotransmitter amino acids glutamate, aspartate and GABA in vivo from the superfused sensori-motor cortex of conscious unanesthetised rats and in vitro from rat cortical synaptosomes. The effects on synaptosomes appear to be due to a depolarising action. Synaptosomal potassium levels were depleted by the toxin. The action was also blocked both in vivo and in vitro by tetrodotoxin and was Ca2+-dependent. The uptake of [U-14C]GABA was inhibited by tityustoxin but this action was prevented by tetrodotoxin (1 microM). Since the release of [U-14C]GABA from synaptosomes due to the tityustoxin was also prevented by tetrodotoxin under identical circumstances, it is concluded that the tityustoxin has a primary action on release of neurotransmitters rather than on uptake.

Animals↗
PubMed1980

Effect of stimulation on the incorporation of 14C from glial and neuronal specific substrates into brain proteins in vivo and in vitro.

The incorporation of amino acids into brain proteins following brachial plexus stimulation (BPS) was studied in anaesthetised Sprague-Dawley rats following injection of radioactive precursors of both neuronal and glial compartments. Following intraperitoneal injection of [14C]glucose, which is the major neuronal pool precursor, BPS resulted in a significant increase of 37% (P < 0.001) in the incorporation of carbon from [14C]glucose into TCA-insoluble proteins in the contralateral sensorimotor cortex as compared with the ipsilateral area of the same animal. This increase was abolished totally when tetrodotoxin (10 micrograms ml-1) was applied topically to the surface of the stimulated area. Following intraperitoneal injection of [14C]acetate, which is considered to by mainly a glial cell precursor, the same afferent electrical stimuli caused a significant decrease of 21% in the incorporation of amino acids into proteins in the stimulated versus unstimulated sensorimotor cortex. With [4-(3)H]phenylalanine or [1-(14)C]leucine as precursors a significant decrease (12%) or no change was recorded, respectively. A similar decrease in protein synthesis in the stimulated sensorimotor cortex was achieved using different routes of injection. No significant changes were observed in the ratio of the specific radioactivities of the total amino acids of the two hemispheres using either precursor. In vitro, synaptosomes showed a large increase in incorporation into proteins after treatment with electrical pulses, both with [14C]glucose and with [U-14C]acetate as precursors.

Acetates↗