Browsing by Author "GALLEGUILLOS, X"

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    BRADYKININ MODULATES THE RELEASE OF NORADRENALINE FROM VAS-DEFERENS NERVE-TERMINALS
    (1991) LLONA, I; GALLEGUILLOS, X; BELMAR, J; HUIDOBROTORO, JP
    To assess whether bradykinin influences the release of noradrenaline from the adrenergic varicosities of the vas deferens, tissues were loaded with 3H-noradrenaline. Upon electrical depolarization bradykinin increased in a concentration-dependent fashion, the overflow of tritium from the mouse or rat vas deferens. The 3H-overflow is dependent on the external Ca2+ concentration suggesting neuronal release of 3H-noradrenaline. The present results add evidence to the hypothesis that bradykinin modulates the release of noradrenaline from peripheral sympathetic nerve terminals via the activation of a presynaptic mechanism.
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    CHANGES IN NORADRENERGIC VESICLE MARKERS OF RABBIT OVIDUCTS DURING PROGESTERONE TREATMENT
    (1983) BELMAR, J; LARA, H; GALLEGUILLOS, X
    The effect of progesterone (P) on norepinephrine (NE), [3H]norepinephrine ([3H]NE) and dopamine .beta.-hydroxylase (DBH) in noradrenergic vesicles from rabbit oviducts was studied after daily injections of the hormone during different periods (4, 7 and 15 days). Progesterone induced a concomitant increase in NE and DBH activity and [3H]NE uptake. To study the mechanism involved in such effects, 4 tissue fractions were obtained by differential centrifugation of the oviducts of which the vesicular fraction was applied over continuous sucrose gradients (0.3-2 M). The changes induced by P in markers of tissue and gradient fractions showed an increase of the NE storage capacity which could be ascribed to an increase in the number of storage vesicles, and/or to a higher extravesicular storage capacity. The occurrence of these mechanisms during pregnancy or after P treatment could account for the (long-lasting) high levels of NE observed in such instances.
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    EFFECT OF CASTRATION AND TESTOSTERONE ON NOREPINEPHRINE STORAGE AND ON THE RELEASE OF [H-3]NOREPINEPHRINE FROM RAT VAS-DEFERENS
    (1985) LARA, H; GALLEGUILLOS, X; ARRAU, J; BELMAR, J
    Norepinephrine and dopamine-.beta.-hydroxylase, used as noradrenergic vesicle markers, were decreased in the rat vas deferens 10 days after castration. Five days of testosterone administration to castrated animals increased the enzyme activity over that of controls but did not modify norepinephrine content. In tissue fractions obtained by differential centrifugation, the highest activities of the noradrenergic markers appeared in the vesicular fraction of controls and in the soluble fraction of castrated animals. Testosterone reversed the effect of castration: it increased dopamine-.beta.-hydroxylase activity in the vesicular and soluble fractions, while norepinephrine increased only in the vesicular fraction. Results obtained after continuous sucrose gradient centrifugation of vesicular fractions suggested that these changes principally affected the number of light noradrenergic vesicles while testosterone increased the number of vesicles reduced by castration. Hormonal manipulations also modified some functional properties of nerve endings: norepinephrine depletion after transmural stimulation in the presence of tetraethylammonium, as well as the release of the neurotransmitter, were decreased after castration. These effects were reversed by testosterone. A modulatory effect of testosterone on the norepinephrine storage system and on the functional properties of the adrenergic innervation of vas deferns is suggested.
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    EFFECT OF CLONIDINE EARLY IN LIFE ON BRAIN MORPHOFUNCTIONAL DEFICITS INDUCED BY NEONATAL MALNUTRITION IN THE RAT
    (1989) SOTOMOYANO, R; HERNANDEZ, A; PEREZ, H; RUIZ, S; GALLEGUILLOS, X; BELMAR, J
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    RELEASE OF H-3 NORADRENALINE FROM THE RAT OVIDUCT - CHANGES DURING ESTROUS-CYCLE AND BY PROGESTERONE INVITRO
    (1990) CHIAPPE, P; GALLEGUILLOS, X; LARA, H; FUENTEALBA, B; FORRAY, I; BELMAR, J
    Rat oviduct noradrenergic innervation seems to be under the influence of hormonal modulation. Noradrenaline level is specifically affected, but other processes like the release of the neurotransmitter have not yet been studied. In this work the release of 3H-noradrenaline (3H-NA) during the estrous cycle and its modification by progesterone "in vitro", were studied. The basal 3H-NA outflow was unchanged during the estrous cycle. However, the induced release (K+, 80 mM) was maximal during estrous. After progesterone, induced 3H-NA release was inhibited at low concentrations (5 .mu.M); under higher concentrations (50 .mu.M) the effect persisted but basal outflow of radioactivity was increased. The inhibitory effect was potentiated by RU-486 (Progesterone blocker). Results suggest a modulatory role for the hormone and it could be related to interactions with nerve-ending membranes and not with classical nuclear receptors.
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    YOHIMBINE EARLY IN LIFE ALTERS FUNCTIONAL-PROPERTIES OF INTERHEMISPHERIC CONNECTIONS OF RAT VISUAL-CORTEX
    (1991) SOTOMOYANO, R; HERNANDEZ, A; PEREZ, H; RUIZ, S; GALLEGUILLOS, X; BELMAR, J
    It has been shown that noradrenaline (NA) is an important regulator of normal regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. The present study was designed to investigate whether enhanced NA release induced by chronic yohimbine administration early in life may alter in the rat the normal pattern of functional interhemispheric connections of the visual cortex. Yohimbine administration to rats between days 5 and 16 of postnatal life (2.5 mg/kg, IP, daily) resulted in changes in the pattern of transcallosal responses evoked in the visual cortex, characterized by a reduction in the peak-to-peak amplitude as well as a reduction of the extent of projecting fields of maximal activity, when examined at 30-35 days following termination of the drug treatment regimen. The results indicate that yohimbine treatment early in life induces functional alterations in the interhemispheric connectivity of the visual areas, probably by disrupting the normal trophic role of NA during synaptogenesis.