Effects of sodium-deficient media and of a calcium ionophore (A-23187) on the release of (3H)-noradrenaline, (14C)-α-aminoisobutyrate, and (3H)-γ-aminobutyrate from superfused slices of rat neocortex (original) (raw)
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The Journal of physiology, 1974
1. Perfusing bovine adrenal glands with Na(+)-free Locke solution for 15-40 min did not modify the increase in the release of catecholamines from glands stimulated by acetylcholine. However, after 80-100 min of perfusion with Na(+)-free solution, the response to acetylcholine stimulation was decreased or abolished.2. Immediately after switching the perfusion medium to Na(+)-free solution, there was a sharp increase (6-10 times over control values) in catecholamine output.3. Graded substitution of Na(+) in the perfusion fluid enhanced the output of catecholamines. This increase in the output of amines was linearly related to the logarithm of the extracellular Na(+) concentration.4. The release of catecholamines in the absence of Na(+) was not reduced by the presence of atropine and hexamethonium nor by the omission of Ca(2+) in the presence of EDTA or EGTA.5. Excess of Mg(2+) in the perfusion fluid reduced (10 mM-Mg(2+)) or blocked (20 mM-Mg(2+)) the increase in the output of catecho...
Neurochemistry International, 1986
AMtraet-The efltux of [3H]noradrenaline (NA) and of the non transmitter, non metabolizable, amino acid [14C]ct-aminoisobutyrate (AIB), was followed simultaneously from superfused rat brain cortex thin slices, that had been preloaded with those substances. Short (2 min) "pulses" of increasing veratridine concentrations were applied at 10 min intervals. When calcium in the superfusion fluid was 1 mM, [3H]NA efflux increased progressively with pulses of I, 3, 10 and 30 aM veratridine, but further increase to 100 #M resulted in a decrease of the induced 3H-efflux. Veratridine-enhanced [3H]NA efllux decreased considerably in 0.I mM calcium and was virtually suppressed when no calcium was added to the superfusion fluid. In l mM calcium, the etltux of [t4C] AIB was increased progressively by pulses of 10, 30 and 100/tM veratridine, but no increase in ettlux was seen with 1 or 3 #M drug. In 0.1 mM, or without added calcium, the induced efflux of [14C]AIB was markedly increased. Similar findings were seen when a long (10 min) pulse of 10 #M veratridine was given. After such long pulses there was a rapid return of AIB effiux to pre-veratridine levels if calcium was 1 mM, but in the absence of added calcium, the return to baseline levels of both [3H]NA and, especially, that of [J4C]AIB efllux, was greatly impaired. The veratridine enhanced efflux of both NA and AIB was entirely blocked by I pM tetrodotoxin.
Neuroscience, 1977
The effect of an elevated concentration (46 mM) of extracellular potassium on the release, from superfused rat brain cortex slices, of labelled y-aminobutyrate, glutamate, glycine, r-and /Galanine, aspartate, taurine and a-aminoisobutyrate has been studied; and a comparison made with the release of soluble (non-vesicular) noradrenaline (i.e. that transported into slices taken from the brains of animals pretreated with reserpine; the slices were incubated with nialamide). In all cases, with the possible exception of L-cc-alanine, elevated potassium induced an increased efflux of these substances. Omission of calcium in the superfusing fluid markedly diminished the release of all the test substances, except, in part, that of /3-alanine. It was also found that the time course of the induced efflux varied considerably for the different substances: substances such as noradrenaline and y-aminobutyrate that are transported predominantly into axons and axon terminals, showed a 'peak' time course, with a maximal release within 24min following potassium elevation, and the rate of release diminished rapidly in spite of the continued presence of high potassium. Such a decreased release was not due to exhaustion of the tissue stores of these substances. On the other hand, glutamate and glycine, substances that are thought to be transported predominantly into glial cells, attained their maximal release rates only 10 min after potassium was elevated, and such release was maintained without decrement. jl-alanine showed a mixed type of release, with a small initial peak resembling that of the axonally located substances, and a delayed release similar to that of glycine and glutamate. The release of the rest of the amino acids also resembled that of glycine and glutamate. A correlation was found (r = 0.99, P < 0.01) between the area of the efflux curve that had a 'peak' shape, and the percentage of the substance that was transported into an axonal compartment.
European Journal of Neuroscience, 1994
We compared the effectiveness of Ca2+ entering by Na+/Ca2+ exchange with that of Ca2+ entering by channels produced by membrane depolarization with K+ in inducing catecholamine release from bovine adrenal chromaffin cells. The Ca2+ influx through the Na+/Ca2+ exchanger was promoted by reversing the normal inward gradient of Na+ by preincubating the cells with ouabain to increase the intracellular Na+ and then removing Na+ from the external medium. In this way we were able to increase the cytosolic free Ca2+ concentration ([Ca2+]c) by Na+/Ca2+ exchange to 325 ± 14 nM, which was similar to the rise in [Ca2+]c observed upon depolarization with 35 mM K+ of cells not treated with ouabain. After incubating the cells with ouabain, K+ depolarization raised the [Ca2+]c to 398 ± 31 nM, and the recovery of [Ca2+]c to resting levels was significantly slower. Reversal of the Na+ gradient caused an −6-fold increase in the release of noradrenaline or adrenaline, whereas K+ depolarization induced a 12-fold increase in noradrenaline release but only a 9-fold increase in adrenaline release. The ratio of noradrenaline to adrenaline release was 1.24 ± 0.23 upon reversal of the Na+/Ca2+ exchange, whereas it was 1.83 ± 0.19 for K+ depolarization. Reversal of the Na+/Ca2+ exchange appeared to be as efficient as membrane depolarization in inducing adrenaline release, in that the relation of [Ca2+]c to adrenaline release was the same in both cases. In contrast, we found that for the same average [Ca2+]c, the Ca2+ influx through voltage-gated channels was much more efficient than the Ca2+ entering through the Na+/Ca2+ exchanger in inducing noradrenaline release from chromaffin ceils. This greater effectiveness of membrane depolarization in stimulating noradrenaline release suggests that there is a pool of noradrenaline vesicles which is more accessible to Ca2+ entering through voltage-gated Ca2+ channels than to Ca2+ entering through the Na+/Ca2+ exchanger, whereas the adrenaline vesicles do not distinguish between the source of Ca2+.
General pharmacology, 1994
1. The release and the metabolism of [3H]noradrenaline ([3H]NA) induced by tyramine was studied in the superior cervical ganglion (cell bodies) and in the nictitating membrane (nerve endings) of the cat. 2. Exposure of the ganglia to 58.0 and 174.0 microM tyramine resulted in the release of 13.7 and 11.8% respectively of the total tissue radioactivity. In the nictitating membrane, the fractional release of radioactivity was directly proportional to the concentration of tyramine (5.8, 58.0 and 174.0 microM). 3. In ganglia [3H]DOPEG accounted for 55.8% of the radioactivity released by 58.0 microM tyramine and only 10.5% of the radioactivity was unmetabolized NA. In presence of 174.0 microM tyramine, [3H]NA increased to 28.0% of the total radioactivity and [3H]DOPEG and [3H]OMDA decreased to 45.3 and 18.9% respectively. 4. In the nerve endings, the contribution of [3H]NA, [3H]DOMA and [3H]NMN increased with the concentration of tyramine while [3H]DOPEG decreased. 5. The deamination is ...