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S Villanueva

Publications and source records attributed to S Villanueva.

32 records · Page 2Linked to original sources
PubMed1988

Veratridine-induced release of endogenous glutamate from rat brain cortex slices: a reappraisal of the role of calcium.

The efflux of endogenous glutamate from thin slices of rat brain cortex superfused in vitro with artificial cerebrospinal fluid (ACSF) was studied. Initially, glutamate efflux was very high (2.5 nmol/mg protein/min), possibly because of the cutting procedure, but declined sharply, and at 30 min of superfusion was 25 pmol/mg protein/min. In ACSF without added calcium, spontaneous glutamate efflux was always higher than that in calcium-containing medium, e.g. at 30 min it was 75 pmol/mg protein/min. Addition of 10 microM veratridine for 2 min, between 30 and 32 min of superfusion, led, in ACSF with calcium, to an increase in glutamate efflux of 288%, when the maximum efflux following veratridine is compared to the glutamate efflux that immediately preceded the application of this drug (from 25 to 97 pmol/mg protein/min), while in ACSF without added calcium, veratridine induced an increase of only 117% (from 75 to 163 pmol/mg protein/min). These results are interpreted as due to the dual effect of veratridine. In calcium-containing ACSF, veratridine increases sodium influx which depolarizes the neurons and opens voltage-sensitive calcium channels. The increased intraneuronal calcium induces glutamate release from synaptic vesicles, while increased intracellular sodium enhances the release of soluble cytoplasmic glutamate by the reverse operation of the plasma membrane, sodium-dependent glutamate carrier. In ACSF without calcium, the release of vesicular glutamate is suppressed, while the sodium-dependent mechanism remains. This appears as if veratridine-induced glutamate efflux were only partially calcium-dependent.

Animals↗
PubMed1988

Endogenous ligands for the quisqualate receptor: presence in rat brain cortex synaptic vesicles.

The presence in highly purified rat brain cortex synaptic vesicles of endogenous ligands for rat brain quisqualate receptors was investigated. The vesicles were extracted, and their contents fractionated by high voltage electrophoresis. Endogenous ligands were detected by a radioreceptor assay in which such ligands competed with 50 nM L-[3H]glutamate for binding to quisqualate receptors present in rat brain postsynaptic densities (PSDs). Binding of L-[3H]glutamate to N-methyl-D-aspartate (NMDA) receptors, also present in PSDs, was blocked by 100 microM NMDA. We found that the endogenous ligands present in brain cortex synaptic vesicles for quisqualate receptors, were glutamate and aspartate, in a molar ratio of about two to one. The quisqualate receptor had an affinity 130-fold higher for glutamate (Kd 0.3 microM) than for aspartate, and the latter amino acid also showed a marked negative cooperative for binding (Hill number 0.29, against 0.67 for glutamate). These findings suggest that glutamate is the natural transmitter that activates quisqualate receptors at some central excitatory synapses, and also that aspartate may be a classical transmitter, the receptor for which still remains to be shown.

Animals↗
PubMed1987

The action of hormones on the rat uterus and mammary gland gamma-glutamyltranspeptidase activity.

The gamma-glutamyltranspeptidase activity of rat uterus and mammary gland was studied in ovariectomized, hypophysectomized and ovariectomized-hypophysectomized rats under different hormonal and drug treatments. The uterine enzyme appears to be mainly dependent on a direct action of estradiol and the mammary gland enzymatic activity is dependent on prolactin. Our result, however, do not exclude a possible role of estradiol in the regulation of prolactin effects on mammary gland enzymatic activity.

Animals↗
PubMedDate not supplied

Thyrotoxic periodic paralysis in Mexican mestizo patients: a clinical, biochemical and HLA-serological study.

BACKGROUND: Thyrotoxic periodic paralysis (TPP) is characterized by episodes of neuromuscular weakness occurring in the context of hypokalemia and hyperthyroidism and has been predominantly described in Oriental populations. Whereas it is uncommon in Caucasians and Blacks, TPP does occur in individuals of Native American descent. The objective was to analyze the clinical, biochemical, and HLA characteristics of a group of Mexican mestizo patients with TPP. METHODS: The sample was comprised of 14 men with TPP diagnosed since January 1990, based on one or more episodes of flaccid paralysis, accompanied by hypokalemia and occurring in the context of clinical and biochemical hyperthyroidism. Eight were available for HLA testing. RESULTS: Hyperthyroidism was diagnosed before the development of periodic paralysis in five of the patients, whereas in six it occurred afterward. The severity of paralysis did not correlate with the degree of either hypokalemia or hyperthyroidism. An increased frequency of HLA-DR3 was found in Graves' patients without paralysis but not in those with paralysis, as compared to the general population. CONCLUSIONS: TPP is more common than previously thought in Mexicans, in whom it behaves as in other Native American groups. The lack of HLA-DR3 association in Graves' patients with TPP is interesting, but at the moment has no pathophysiological implications.

Adult↗
PubMedDate not supplied

Postnatal thyroxine supplementation in infants less than 32 weeks' gestation: effects on pulmonary morbidity.

OBJECTIVE: Transient hypothyroxinemia in premature newborns has been linked with poor neonatal outcomes. We designed this study to evaluate the effects of early thyroxine (T4) administration in the premature infant. STUDY DESIGN: A total of 49 newborns less than 32 weeks' gestation, were randomized in a double-blind, placebo-controlled trial. Within the first 48 hours of life, T4 (10 or 20 micrograms/kg; intravenous or through nasogastric tube, respectively) was administered for a total of 21 days. Chronic lung disease, the primary outcome variable, was defined by oxygen dependency at 28 days of life. RESULTS: The incidence of chronic lung disease, death, grade III or IV intraventricular hemorrhage, periventricular leukomalacia, and sepsis was not different in the placebo and treated groups. CONCLUSION: Early T4 supplementation in preterm newborns less than 32 weeks' gestation does not decrease the incidence of chronic lung disease or other complications of prematurity.

Bronchopulmonary Dysplasia↗