ArticleNeurochemical research2004
Influence of hypotonic shock on glutamate and GABA uptake in rat brain synaptosomes.
Article in Neurochemical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 15 citations in OpenAlex.
- Influence of intra- and extracellular acidification on free radical formation and mitochondria membrane potential in rat brain synaptosomes.Journal of molecular neuroscience : MN · 2013Article
- Presynaptic glycine receptors influence plasma membrane potential and glutamate release.Neurochemical research · 2010Article
- Influence of integrin-blocking peptide on gadolinium- and hypertonic shrinking-induced neurotransmitter release in rat brain synaptosomes.Neurochemical research · 2008Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Hyponatremia leads to hyperexcitability of neurons, seizures, and coma. It is well established that uptake of neurotransmitters is a sodium-dependent process. Therefore, we suggest that inhibition of neurotransmitter uptake can lead to the clinical manifestations of hyponatremia. Decreasing of sodium concentration down to 92 mM in incubation medium, which corresponds to lowering the osmolarity down to 230 mOsm/l, leads to a 45% decrease in glutamate uptake and a 46% decrease in gamma-aminobutyric acid (GABA) uptake. However, this effect was mediated by the nonspecific lowering of osmolarity rather than by decreasing sodium concentration. Hypotonic shock was able to reduce glutamate uptake in the presence of protein kinase inhibitors staurosporine and genistein, the phosphatase inhibitor okadaic acid, the phosphatidylinositol 3-kinase inhibitor wortmannin, and cytoskeleton modulators colchicine and cytochalasin B. Therefore, we suggest that intracellular signaling is not mediating the effect of osmolarity reduction on neurotransmitter uptake.
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