GABA, Hypotaurine and Taurine Transport in Brain Slices from Developing Mouse

J of Neuroscience Research

Saransaari

1992

The release of preloaded radiolabeled taurine was studied in superfused cerebral cortex slices obtained from adult and 3-day-old mice in media of varying ionic composition. Our aim was to establish whether the release of taurine from slices evokable by high concentrations of K+ could be attributed solely to cell volume changes or whether it results directly from depolarization of cell membranes. In both age groups hypoosmotic media enhanced the release of taurine. The enhancement was greater in 3-day-old than in adult mice. The K(+)-evoked release of taurine was likewise greater in slices from 3-day-old mice than in slices from adult mice. The K+ stimulation was totally preserved in adult mice and partially preserved in 3-day-old mice when the slices were superfused with Cl(-)-free media, with media in which the K+ x Cl- ionic product was kept constant and with hyperosmotic high-K+ media. The results were practically the same when the permeant anion acetate and the impermeant anion gluconate were used to replace the Cl- deficit. The unstimulated release of preloaded taurine was greatly enhanced in Cl(-)-free media in both age groups. There obtained no statistically significant correlation between the intracellular swelling of slices and the magnitude of taurine release under the present different experimental conditions in either age group. The results show that the K(+)-evoked release of taurine from superfused cerebral cortex slices cannot be solely attributed to depolarization-induced cell swelling. At least a part of the release results directly from membrane depolarization which besides exocytosis apparently also enhances the carrier-mediated release of taurine and inhibits the reuptake of taurine liberated from intracellular compartments.

Section: Discussionmentioning

confidence: 99%

Taurine release and swelling of cerebral cortex slices from adult and developing mice in media of different ionic compositions

J of Neuroscience Research

Saransaari

1992

“…Sodium-dependent high-and low-affinity GABA uptake systems have been shown to operate in nervous tissue in both adult and developing mice. 39 If the cell membrane is depolarized and/or the Na-gradient diminished, j7 the direction of transport changes from inward (uptake) to outward (release). This Ca-independent release has been claimed to be activated in pathological conditions, including anoxia.…”

Section: Mechanism(s) Of Ischemia-induced Releasementioning

confidence: 99%

Enhanced GABA release in cell‐damaging conditions in the adult and developing mouse hippocampus

Saransaari

Intl J of Devlp Neuroscience

1997

The release of [3H]GABA from hippocampal slices from adult (3-month-old) and developing (7-day-old) mice was studied in cell-damaging conditions in vitro using a superfusion system. Cell damage was induced by modified superfusion media, including hypoxia, hypoglycemia, ischemia, the presence of Free radicals and oxidative stress. The basal release of GABA from the immature and mature hippocampus was generally markedly increased in all cell-damaging conditions. In 7-day-old mice the release was enhanced most in the presence of free radicals. 1.0 mM NaCN and ischemia, whereas in the adults 1.0 mM NaCN provoked the largest release of GABA, followed by ischemia and free radical-containing media. Potassium stimulation (50 mM K+) was still able to potentiate the release in all cell-damaging conditions in both age groups. It was shown by superfusing the slices in Ca- and Na-free media that ischemia-induced GABA release was Ca-independent, occurring by a reversed operation of Na-dependent cell membrane carriers in both adult and developing hippocampus. Glutamate and its receptor agonists, N-methyl-D-aspartate (NMDA), kainate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), potentiated GABA release only in the immature hippocampus by a receptor-mediated mechanism. The enhancement by kainate and AMPA receptors also operated under ischemic conditions. The massive amount of GABA released simultaneously with excitatory amino acids in the mature and immature hippocampus may be an important protective mechanism against excitotoxicity, counteracting harmful effects that lead to neuronal death. The GABA release induced by activation of presynaptic glutamate receptors may contribute particularly to the maintenance of homeostasis in the hippocampus upon impending hyperexcitation.

“…The concentration of y-aminobutyric acid (GA4BA) increases with the maturation of the mouse hain, whereas the level of taurine is very high in the developing brain and decreases toward adulthood (e.g., Kontro et al, 1984). In the murine cerebral cortex the number of synapses increases severalfold during the second and third postnatal weeks (Purves and Lichtman, 1985).…”

mentioning

confidence: 99%

Release of Endogenous Taurine and γ‐Aminobutyric Acid from Brain Slices from the Adult and Developing Mouse

Journal of Neurochemistry

Kontro

1989

The spontaneous and potassium-stimulated release of endogenous taurine and gamma-aminobutyric acid (GABA) from cerebral cortex and cerebellum slices from adult and developing mice was studied in a superfusion system. The spontaneous release of GABA was of the same magnitude in slices from adult and developing mice, but the spontaneous release of taurine was considerably greater in the adults. The potassium-stimulated release of GABA from cerebral cortex slices was about five times greater in adult than in 3-day-old mice, but the potassium-stimulated release of taurine was more than six times greater in 3-day-old than in adult mice. In cerebellar slices from 7-day-old mice, potassium stimulation also evoked a massive release of taurine, whereas the evoked release from slices from adult mice was rather negligible. Also in cerebellar slices the potassium-stimulated release of GABA exhibited the opposite quantitative pattern. The stimulated release of both GABA and taurine was partially calcium dependent. The results suggest that taurine may be an important regulator of excitability in the developing brain.