Changes in Free Fatty Acids of Brain by Drug‐induced Convulsions, Electroshock and Anaesthesia

Bazan, N.G.

doi:10.1111/j.1471-4159.1971.tb00002.x

Cited by 180 publications

(38 citation statements)

References 20 publications

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“…Ischemia and related situations are known to stimulate phospholipases, enzymes that attack membrane phospholipids (Bazan, 1970(Bazan, ,1971. A major role in the degradation of membranes is at tributed to phospholipase A 2 • This enzyme requires the presence of Ca 2 + for hydrolysis of phosphati dylcholine (Edgar and Freysz, 1982).…”

Section: Discussionmentioning

confidence: 99%

Formation of Free Choline in Brain Tissue during in vitro Energy Deprivation

Djuričić

Olson

Assaf

et al. 1991

J Cereb Blood Flow Metab

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Summary: Free choline and ATP contents were mea sured in Mongolian gerbil hippocampal slices (tissue) and incubation media (media) during exposure to 30 min of aglycemia, high potassium, anoxia, or ischemia. Changes in choline levels reflected the degree of energy reduction, lower ATP levels being associated with high choline (4-fold increase during exposure to high potassium and an oxia, and II-fold increase during ischemia). Media (ex tracellular) choline was particularly affected and in creased about twofold during relatively mild energy depletion (e.g., aglycemia), but tissue choline content was less sensitive to energy reduction. A plot of choline vs. ATP levels indicated a nonlinear correlation, and the sharp increase in choline occurred when ATP values fell Choline is a precursor not only for acetylcholine, but also for phospholipids (phosphatidylcholine) and sphingomyelin in the brain. Thus, choline is involved in two important aspects of brain function: neurotransmission and the maintenance of cell membrane integrity. Both aspects are affected by a decrease in energy reserves. Synthesis and storage of acetylcholine are glucose and energy dependent (Gibson and Blass, 1976;Yamagata and Parsons, 1989) 308to about 2.5 nmollmg of protein. Inhibition of acetylcho line sterase by \0 fLM physostigmine during ischemia did not prevent an increase in choline contents but rather enhanced them, indicating that acetylcholine hydrolysis was not the source of free choline. Formation of free choline was Ca 2 + independent. These findings suggest the involvement of phospholipase D and phosphatidyl choline hydrolysis in free choline formation during energy stress. The extent of choline formation may be an indi cator of the degree of membranal damage, which in turn reflects damage to the metabolic machinery of the cell.

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Section: Discussionmentioning

confidence: 99%

Formation of Free Choline in Brain Tissue during in vitro Energy Deprivation

Djuričić

Olson

Assaf

et al. 1991

J Cereb Blood Flow Metab

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“…Experimental brain ischaemia and reperfusion 14, animal model of amyotrophic lateral sclerosis 15 and experimental seizures 16 have been shown to influence several of the aforementioned substances.…”

Section: Introductionmentioning

confidence: 99%

Severity of experimental traumatic brain injury modulates changes in concentrations of cerebral free amino acids

Amorini

Lazzarino

Pietro

et al. 2016

J Cellular Molecular Medi

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In this study, concentrations of free amino acids (FAA) and amino group containing compounds (AGCC) following graded diffuse traumatic brain injury (mild TBI, mTBI; severe TBI, sTBI) were evaluated. After 6, 12, 24, 48 and 120 hr aspartate (Asp), glutamate (Glu), asparagine (Asn), serine (Ser), glutamine (Gln), histidine (His), glycine (Gly), threonine (Thr), citrulline (Cit), arginine (Arg), alanine (Ala), taurine (Tau), γ‐aminobutyrate (GABA), tyrosine (Tyr), S‐adenosylhomocysteine (SAH), l‐cystathionine (l‐Cystat), valine (Val), methionine (Met), tryptophane (Trp), phenylalanine (Phe), isoleucine (Ile), leucine (Leu), ornithine (Orn), lysine (Lys), plus N‐acetylaspartate (NAA) were determined in whole brain extracts (n = 6 rats at each time for both TBI levels). Sham‐operated animals (n = 6) were used as controls. Results demonstrated that mTBI caused modest, transient changes in NAA, Asp, GABA, Gly, Arg. Following sTBI, animals showed profound, long‐lasting modifications of Glu, Gln, NAA, Asp, GABA, Ser, Gly, Ala, Arg, Citr, Tau, Met, SAH, l‐Cystat, Tyr and Phe. Increase in Glu and Gln, depletion of NAA and Asp increase, suggested a link between NAA hydrolysis and excitotoxicity after sTBI. Additionally, sTBI rats showed net imbalances of the Glu‐Gln/GABA cycle between neurons and astrocytes, and of the methyl‐cycle (demonstrated by decrease in Met, and increase in SAH and l‐Cystat), throughout the post‐injury period. Besides evidencing new potential targets for novel pharmacological treatments, these results suggest that the force acting on the brain tissue at the time of the impact is the main determinant of the reactions ignited and involving amino acid metabolism.

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“…Free arachidonic acid can increase by 40 J.Lglg of tissue after 3 min of brain ischaemia. Eleva tion of free arachidonic acid levels also occurs with cerebral trauma, seizures, and electroshock (Bazan , 1970(Bazan , , 1971. Phospholipase A2 may be the rate limiting step in the formation of prostaglandins by controlling the supply of the precurser, arachidonic ac id (Flower and Blackwell, 1976).…”

Section: Cerebral Arachidonic Acid Metabolismmentioning

confidence: 99%