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H Pasantes-Morales

Publications and source records attributed to H Pasantes-Morales.

At least 91 records · Page 5Linked to original sources
PubMed1989

Potassium-stimulated release of [3H]taurine from cultured GABAergic and glutamatergic neurons.

The effect of depolarizing concentrations of potassium (56 mM) on the release of [3H]taurine was examined in two types of cultured neurons from mouse brain: cerebral cortex neurons, which are largely GABAergic, and cerebellar neurons, which after treatment with kainate consist almost entirely of glutamatergic granule cells. The release of [3H]taurine was compared to that of gamma-[3H]aminobutyric acid [( 3H]GABA) in cortical neurons and to that of D-[3H]aspartate in granule cells. Cortical neurons responded to potassium stimulation (1 min or continuously) by an immediate increase in [3H]GABA efflux of more than six times over the basal efflux, followed by a sharp decline despite the persistence of the stimulatory agent. The potassium-induced release of [3H]GABA was largely calcium-dependent. The release of [3H]taurine was considerably less in magnitude, only doubling after the stimulus, with a time course delayed in both onset and decline. The release of [3H]taurine was partially calcium-dependent and was also decreased in low-chloride solutions. In cerebellar granule cells, exposure to potassium resulted in a large (sixfold) and prompt release of D-[3H]aspartate, largely calcium-dependent. A totally different pattern was observed for the release of [3H]taurine. A stimulatory effect occurred only when cells were exposed continuously to potassium. Taurine efflux was very delayed, with a broad stimulus plateau reached after 15-20 min of stimulation. Taurine release was unaffected by omission of calcium, but it was abolished in a low-chloride medium. These results suggest that taurine is released from cells handling other neuroactive amino acids as neurotransmitters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A chloride-dependent component of the release of labeled GABA and taurine from the chick retina.

The characteristics and ionic dependence of the release of [3H]gamma-aminobutyric acid ([3H]GABA) and [3H]taurine from the chick retina, stimulated by kainic acid (KA) and by depolarizing concentrations of potassium was examined and compared to those of [3H]dopamine. KA (100 microM) highly stimulated the release of [3H]GABA (25-fold over resting efflux), induced a moderate increase in [3H]taurine and did not increase the efflux of [3H]dopamine. The efflux of [3H]GABA stimulated by KA was totally calcium-independent but it was markedly sodium and chloride dependent. Chloride dependence was assessed by replacing chloride with the impermeant anion gluconate, or by addition of the anion transport blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). Depolarizing concentrations of KCl (56 mM) stimulated the release of [3H]GABA, [3H]taurine and [3H]dopamine to about the same extent. The release of [3H]GABA and [3H]taurine was only partially calcium dependent, in contrast to the highly calcium-dependent efflux of [3H]dopamine. A sodium-free medium increased the resting efflux and decreased the potassium-stimulated release of [3H]GABA and [3H]taurine; the resting efflux of [3H]dopamine was unaffected and the potassium-induced efflux was somewhat increased. The potassium-stimulated efflux of [3H]GABA and [3H]taurine showed a chloride-dependent component which was higher for taurine whereas the resting efflux was not modified. The stimulated release of [3H]dopamine was increased in a chloride-free medium. The ionic dependence of KA and potassium stimulated efflux of [3H]GABA and [3H]taurine showed properties similar to those of the homoexchange-activated efflux of amino acids which was also found sodium and chloride dependent and clearly different from the calcium-coupled neurotransmitter release process. Exposure of retinas to KA and potassium produced retinal cell swelling which is prevented in a chloride-free medium. Results are discussed in terms of a particular efflux mechanism for [3H]GABA and [3H]taurine in the retina in response to stimulation associated with changes in ionic gradients and retinal cell swelling.

Animals↗
PubMed1988

Taurine and nifedipine protect retinal rod outer segment structure altered by removal of divalent cations.

A protective effect of taurine on morphological alterations induced in isolated ROS by remotion of divalent cations is described. ROS damage is not observed when sodium or chloride is replaced by impermeant ions or in the presence of nifedipine (10 microM). An increased accumulation of 22Na but not of 36Cl occurs in retinas incubated in divalent cation free medium. Taurine (5-25 mM) provides a concentration-dependent protection to ROS structure. Taurine is also able to reduce the increased 22Na influx to control values. These results suggest a protective action of taurine probably involving an interaction with calcium sites on ROS membranes which regulate sodium permeability.

Amino Acids↗
PubMed1988

Effect of light deprivation on the ERG responses of taurine-deficient rats.

The decrease of taurine levels in the retina of taurine-depleted rats treated with guanidinoethane sulfonate (GES) reduced the amplitude of the a- and b-waves of the electroretinogram, registered as a function of the log relative intensity stimulus. The effect was observed either in rats exposed to a light-darkness cycle or to continuous darkness; this effect was somewhat more pronounced in retinas of rats exposed to light. Values obtained from the Naka-Rushton equation for the V-log I curve for the a-wave showed that the half-saturating intensity was unchanged but Vmax was decreased by GES treatment. Implicit times for the b-wave delayed whereas those for the a-wave were unaffected by the treatment.

Animals↗
PubMed1987

Higher susceptibility of taurine-deficient rats to seizures induced by 4-aminopyridine.

The susceptibility of rats made deficient of taurine by treatment with guanidinoethane sulfonate (GES), to seizures induced by 4-aminopyridine was examined. Guanidinoethane sulfonate, at a concentration of 1% was administered to pregnant rats, in the drinking water 2-3 days prior to delivery and the treatment was continued during nursing. Pups were weaned to the same treatment until 6 weeks of age. This treatment decreased levels of taurine in the cerebral cortex by 70%. 4-Aminopyridine was injected intraperitoneally at doses ranging from 4-7 mg/kg. Taurine-deficient rats showed a greater susceptibility to seizures, as demonstrated by a lowered latency for clonic seizures, an increased incidence of tonic seizures and a higher postseizure mortality. These results suggest an involvement of endogenous taurine in nervous excitability.

4-Aminopyridine↗
PubMed1987

Effect of tocopherol and taurine on membrane fluidity of retinal rod outer segments.

The deficiency of taurine and alpha-tocopherol results in disturbances of the structure of retinal rod outer segments. In this study the effect of alpha-tocopherol (vitamin E) and taurine on the fluidity of membranes from frog retinal rod outer segments and of liposomes prepared with lecithin or with lipids from outer segment membranes was examined by steady-state fluorescence polarization of diphenyl-hexatriene (DPH). alpha-Tocopherol increased the DPH anisotropy parameter in both preparations. The vitamin modified the breakpoint temperature of Arrhenius plots of DPH anisotropy, and decreased the activation energy. Taurine failed to modify any of the parameters examined in both outer segment membranes and lecithin liposomes. These results suggest a stabilizer role for tocopherol in rod outer segment membranes. In contrast, the requirement of taurine to maintain outer segment structure seems unrelated to an effect on the physical state of membrane lipids.

Animals↗
PubMed1986

Glutamate receptor agonists release [3H]GABA preferentially from horizontal cells.

A total of 5-6 different cell types in vertebrate retinas accumulate [3H]gamma-aminobutyric acid (GABA). In frog retina, specific populations of cells in the horizontal, amacrine and ganglion cell layers are labeled autoradiographically after a 15-min in vitro incubation with [3H]GABA. Cells which may be bipolar or interplexiform cells are also labeled. Similar autoradiographic patterns are observed in chick retina except for the absence of labeled bipolar or interplexiform cells. In rat retinas, [3H]GABA uptake is limited primarily to Muller and amacrine cells. Depolarizing glutamate receptor agonists (glutamate, aspartate and kainic acid) applied in an in vitro perfusion system, stimulated massive release of [3H]GABA from frog and chick retina but not from rat retina. Under these conditions, autoradiographic labeling of horizontal cells was virtually depleted, while labeling of other cell types remained robust. In contrast, potassium caused release of the label from all 3 types of retina, and loss of autoradiographic labeling occurred uniformly in all cell types. We conclude that [3H]GABA-accumulating horizontal cells possess depolarizing glutamate receptors and that activation of these receptors leads to a release of GABA stores. On the other hand, Muller cells and the various subclasses of [3H]GABA-accumulating amacrine, bipolar and/or interplexiform cells, do not release GABA in response to glutamate receptor stimulation and thus appear to be relatively insensitive to excitatory amino acids.

Animals↗
PubMed1986

Hypotaurine uptake by the retina.

A study of the transport of 3H-hypotaurine by rat retina has been carried out. The process is markedly sodium and temperature dependent. Kinetic analysis of the data revealed two values for the affinity constant (K) of 4.91 microM and 1,071.3 microM. Some related and unrelated amino acids were examined as competitive inhibitors of 3H-hypotaurine transport. Only GABA and beta-alanine exhibited appreciable inhibitory activity. Taurine, glycine, and guanidine ethane sulfonate were not inhibitors. 3H-hypotaurine uptake was similarly distributed in the retinal subcellular fractions P1 and P2. The active uptake of 3H-hypotaurine by retinas of the rat and other species including chick and frog was studied and compared to cerebral cortex slices. The chick retina was similar to the rat in its capacity to transport hypotaurine whereas frog exhibited fourfold less activity. Slices of cerebral cortex from rat and chick exhibited hypotaurine uptake but again the magnitude of the transport was three to fourfold less than in the comparative retinas.

Animals↗
PubMed1986

Pharmacological identification of retinal cells releasing taurine by light stimulation.

The effect of drugs blocking synaptic activity at different retinal levels was examined in this study, in an attempt to identify the origin of the light-stimulated release of 3H-taurine from the chick retina. It was determined by autoradiography that the chick retina accumulates taurine in photoreceptors, in cells from the inner nuclear layer, and in processes of the inner plexiform layer. All these are possible sites for the release of taurine upon illumination. To discriminate among these possibilities, the effects of aspartate, tetrodotoxin, strychnine, picrotoxin, chlorpromazine, tubocurarine, atropine, glutamate diethyl esther, alpha-amino adipate and 2-amino-4-phosphonobutyrate were studied. Aspartate (10 mM), which is known to eliminate the light response of cells postsynaptic to photoreceptors, induced a marked increase of 150% in the resting efflux of 3H-taurine but did not decrease significantly the light-stimulated release. Tetrodotoxin, which blocks amacrine cell responses, decreased 3H-taurine release stimulated by light by less than 20%. The efflux of taurine was unaffected by strychnine, picrotoxin, tubocurarine, atropine, chlorpromazine, and 2-amino-4-phosphonobutyrate, whereas it was increased by glutamate diethyl esther and alpha-amino adipate. These results, all together, point to photoreceptors as the cells releasing 3H-taurine in response to light.

2-Aminoadipic Acid↗
PubMed1986

Inhibitory effect of taurine on 4-aminopyridine-stimulated release of labelled dopamine from striatal synaptosomes.

4-Aminopyridine (4-AP) stimulated the release of [3H]dopamine from striatal synaptosomes in the rat. At a concentration of 200 microM, 4-aminopyridine increased the spontaneous efflux of dopamine by 170%. The effect of 4-aminopyridine was calcium-dependent, being abolished when calcium was omitted from the incubation medium. Taurine, at a concentration of 25 mM, decreased the stimulatory effect of 4-aminopyridine from 170 to 49%, in the presence of 2.5 mM calcium. When the concentration of calcium in the superfusion medium was reduced to 0.1 mM, taurine had a complete inhibitory effect on the release of [3H]dopamine stimulated by 4-aminopyridine. The effect of taurine was dose-dependent. Glycine had no effect on the release of [3H]dopamine stimulated by 4-aminopyridine, either in the presence of absence of calcium, whereas gamma-aminobutyric acid (GABA) showed a slight inhibitory effect in both conditions. The results suggest that taurine antagonizes the release of [3H]dopamine induced by 4-aminopyridine through an effect mediated by calcium.

4-Aminopyridine↗
PubMed1986

Retinal degeneration induced by taurine deficiency in light-deprived cats.

The effect of light deprivation on the retinal degeneration induced by taurine deficiency in cats was examined in this study. After 25 weeks of taurine-free diet, taurine levels in plasma, retina, heart, cerebellar and cerebral cortex decrease to 16-25% of normal. The ERG a-wave and b-amplitudes also decreased as a consequence of the taurine-free diet. After 15 weeks of taurine-free diet the b-wave amplitude decreased to 36-41% of normal, and after 25 weeks both the a-wave and the b-wave were undetectable. The structure of the outer segments of photoreceptors, examined by electron microscopy appeared disturbed in the taurine-deficient cats, showing disorientation of the disk membranes, vesiculation and swelling. The time course of taurine deficiency and the retinal degeneration pattern were observed in all cats fed the taurine-free diet, irrespective of the conditions of lighting. These results indicate that the morphological and functional disturbances induced by taurine deficiency in cats are independent of the physiological stimulation of the retina by light.

Animals↗
PubMed1985

Taurine and hypotaurine inhibit light-induced lipid peroxidation and protect rod outer segment structure.

Exposure of isolated frog rod outer segments to light (5000 lux) induces membrane disorganization and swelling. An increase of about 50% on lipid peroxidation, measured by the extent of malonaldehyde formation, accompanied the light-induced damage. Taurine and hypotaurine (25 mM) prevented the increase in lipid peroxidation, and provided an entire protection of rod outer segment structure.

Animals↗
PubMed1984

Effect of guanidinoethane sulfonate on taurine uptake by rat retina.

Guanidinoethane sulfonate (GES) markedly decreased 3H-taurine accumulated in the retina by the high-affinity uptake process. The effect of GES was dose-dependent. Analysis of the kinetics of GES effect revealed that it is a competitive inhibitor. The uptake of taurine by GES was less affected in rat cerebral cortex slices, where the inhibition by 1 mM GES was only 28%. Taurine accumulation by tissues of rats treated with GES (0.1% and 1% in the drinking water) was found to be particularly decreased in the retina, although accumulation by heart and liver was also affected by the higher dose. Taurine uptake by cerebellum and cerebral cortex slices was unaffected by GES. Treatment of rats with GES is known to produce an alteration in the structure and function of the retina, but apparently not in other organs. We discuss whether the marked effect of GES on taurine transport by the retina is related to the deleterious effect of the inhibitor in this organ.

Animals↗
PubMed1984

Antagonistic effects of taurine and 4-aminopyridine on guinea pig ileum.

The effects of 4-aminopyridine (4-AP) and of taurine on the guinea pig ileum were examined. Four-AP increases the basal activity from 1.3 to 6.45 cm2/min. This effect is atropine-sensitive and calcium-dependent. Taurine counteracts the effects of 4-AP on muscle contracture in a concentration-dependent manner. In muscles preincubated with 20 mM taurine, the effect of 4-AP decreased about 65%. Taurine added at the time of maximal effect of 4-AP reduced the muscle contracture induced by the drug to the basal levels. Glycine and beta-alanine did not influence the contracture induced by 4-AP, whereas 25 mM gamma-aminobutyric acid (GABA) reduced it by 30%. Taurine reduced the basal muscle activity by 50% but did not affect the contracture induced by exogenously applied acetylcholine.

4-Aminopyridine↗