Biochemical Pharmacology of GABA in CNS

Tapia, Ricardo

doi:10.1007/978-1-4684-3174-2_1

Cited by 40 publications

(27 citation statements)

References 317 publications

(251 reference statements)

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“…In our previous studies (Smiatowska, 1980) in which we used two other GABA-ergic compounds: AOAA (GABA-t inhibitor; Gottesfeld et aI., 1972;Tapia, 1975) or etomidate (putative GABA agonist; Evans and Hill, 1977) we obtained similar effects.…”

Section: Discussionsupporting

confidence: 80%

The effect of intraperitoneal injection of GABA or GHBA on monoamine histofluorescence in the rat brain

Śmiałowska

Slusarska

1981

J. Neural Transmission

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Using the Falck-Hillarp histofluorescence method we studied the effect of gamma-aminobutyric acid (GABA) or gamma-hydroxybutyric acid (GHBA) on catecholaminergic (CA) and serotoninergic (5-HT) neurons in the rat brain. Both GABA as well as GHBA enhanced the CA fluorescence in noradrenergic (NA) terminals in the cerebellar cortex, which suggested that the NA content increased in these terminals. GHBA but not GABA also enhanced the fluorescence in dopaminergic (DA) terminals in the neostriatum and limbic structures. No significant changes of fluorescence were found in 5-HT neurons after both compounds. The results obtained suggest that, apart from the known GABA-DA interaction, there exists also a GABA-NA interaction in the cerebellar cortex.

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Section: Discussionsupporting

confidence: 80%

The effect of intraperitoneal injection of GABA or GHBA on monoamine histofluorescence in the rat brain

Śmiałowska

Slusarska

1981

J. Neural Transmission

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“…There is little corresponding postischemic de crease in total tissue GAB A that could be attributed to a high glutamic acid decarboxylase/GABA-trans aminase activity ratio related to persistent acidosis or energy failure during reperfusion (Erecinska et aI., 1984). In addition, the GABA loss from the brain tissue is probably limited due to its poor blood-brain barrier permeability (Tapia, 1975). The rather well-preserved postischemic GABA content could also be related to indications that cellular ele ments with high GABA content are more resistent to ischemia than aspartate/glutamate rich cells (Jo hansen et aI., 1983).…”

Section: Discussionmentioning

confidence: 99%

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Hagberg

Lehmann

Sandberg³

et al. 1985

J Cereb Blood Flow Metab

657

246

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Brain ischemia was induced for 10 or 30 min by clamping the common carotid arteries in rabbits whose vertebral arteries had previously been electrocauterized. EEG and tissue content of high energy phosphates were used to verify the ischemic state and to evaluate the degree of postischemic recovery. Extracellular levels and total contents of amino acids were followed in the hippocampus during ischemia and 4 h of recirculation. At the end of a 30-min ischemic period, GABA had increased 250 times, glutamate 160 times, and aspartate and taurine 30 times in the extracellular phase. The levels returned to normal within 30 min of reflow. A delayed increase of extracellular phosphoethanolamine and ethanolamine peaked after 1–2 h of reflow. Ten minutes of ischemia elicited considerably smaller but similar effects. With respect to total amino acids in the hippocampus, glutamate and aspartate decreased to 30–50% of control while GABA appeared unaffected after 4 h of reflow. Alanine, valine, phenylalanine, leucine, and isoleucine increased severalfold. The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, are considered in relation to the pathophysiology of neuronal cell loss during cerebral ischemia.

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“…a finding which recently has been confirmed by Yamamoto ( 1990). A decreased GABA activity during cyanide intoxication would in part explain the increased susceptibility to convulsions (Tapia 1975).…”

mentioning

confidence: 73%

On the Inhibition of Glutamic Acid Decarboxylase and γ‐Aminobutyric Acid Transaminase by Sodium Cyanide

Cassel

Karlsson

Sellström

1991

Pharmacology & Toxicology

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The effects of sodium cyanide (NaCN) on the gamma-aminobutyric acid metabolizing enzymes glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) were studied in vitro. With no pyridoxal-5-phosphate added, GAD was non-competitively inhibited by NaCN, with an IC50 of 280 microM. GAD was also inhibited when exposed to an equimolar amount of NaCN and pyridoxal-5-phosphate. NaCN inhibited GABA-T. The inhibition kinetics suggests that NaCN may react with more than one of the substrates and products present during the reaction, i.e. pyridoxal-5-phosphate, alpha-ketoglutarate and/or succinic semialdehyde. The presence of pyridoxal-5-phosphate in the reaction mixture completely protected GABA-T from inhibition by NaCN. The gamma-aminobutyric acid synthesizing enzyme, GAD may thus be inhibited in vivo by NaCN or by a reaction product of NaCN and pyridoxal-5-phosphate. The gamma-aminobutyric acid catabolizing enzyme, GABA-T is not as vulnerable to inhibition by NaCN, since the cyanide-pyridoxal-5-phosphate complex is ineffective as inhibitor.

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Biochemical Pharmacology of GABA in CNS

Cited by 40 publications

References 317 publications

The effect of intraperitoneal injection of GABA or GHBA on monoamine histofluorescence in the rat brain

The effect of intraperitoneal injection of GABA or GHBA on monoamine histofluorescence in the rat brain

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

On the Inhibition of Glutamic Acid Decarboxylase and γ‐Aminobutyric Acid Transaminase by Sodium Cyanide

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