Browsing by Author "BITRAN, M"

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    AGE AND CASTRATION MODULATE THE INHIBITORY-ACTION OF NEUROPEPTIDE-Y ON NEUROTRANSMISSION IN THE RAT VAS-DEFERENS
    (1991) BITRAN, M; TORRES, G; FOURNIER, A; STPIERRE, S; HUIDOBROTORO, JP
    The potency of neuropeptide Y (NPY) to inhibit the electrically induced contractions of the epididymal half of the vas deferens diminishes markedly with age, being at least 20 times lower in the adult than in the 26-day-old rat. Castration sensitizes the epididymal segment to NPY in a testosterone-reversible manner. [Pro34]NPY was 3 times less potent than NPY in prepubertal rats and inactive in castrated adults, while NPY-(13-36) had no effect in either group. In the prostatic half, NPY and its analogs were active in rats from all ages studied; the order of potency being NPY > [Pro34]NPY > NPY-(13-36). The sensitivity of the prostatic segment from adult rats to NPY was unchanged by castration or testosterone replacement therapy. The NPY content of the ductus increases during development being higher in,the prostatic than in the epididymal half at all ages studied. Castration decreases the peptide content in the two segments and the effect is prevented by testosterone administration. The present investigation demonstrated that the effect of NPY on vas deferens neurotransmission is subject to regulation by sex steroids, which affects differently the response of the two segments of the ductus.
  • No Thumbnail Available
    Item
    CORELEASE OF NEUROPEPTIDE-Y (NPY) AND NORADRENALINE FROM THE SYMPATHETIC-NERVE TERMINALS SUPPLYING THE RAT VAS-DEFERENS - INFLUENCE OF CALCIUM AND THE STIMULATION INTENSITY
    (1992) TORRES, G; BITRAN, M; HUIDOBROTORO, JP
    Epididymal (E) and prostatic (P) segments of the rat vas deferens were incubated with tritium-labeled noradrenaline (NA); upon transmural electrical stimulation for 20 or 60 s (70 V, 1 ms, 3-35 Hz), the outflow of immunoreactive neuropeptide Y (ir-NPY) and NA was detected in the superfusion media. Ir-NPY was detected only following trains of 35 Hz for 60 s in both E and P. In contrast, tritium was released in a graded fashion following trains of 3, 15 or 35 Hz stimulation for 60 s in E, whereas in P it reached a plateau at frequencies larger than 15 Hz. The outflow of tritium, under present conditions, was dependent on the duration of the stimuli, while the release of ir-NPY was only evoked with stimuli of 60 s duration. In the absence of external Ca2+, neurotransmission was blocked and co-release of ir-NPY and NA was prevented.
  • No Thumbnail Available
    Item
    ON THE MECHANISM OF PRE-SYNAPTIC AUTORECEPTOR-MEDIATED INHIBITION OF TRANSMITTER SYNTHESIS IN DOPAMINERGIC NERVE-TERMINALS
    (1982) BITRAN, M; BUSTOS, G
    The effect of apomorphine (APO) upon dopamine (DA) synthesis and release from rat striatal slices was studied. The synthesis of DA was measured by incubating the slices in Krebs-Ringer phosphate (KRP) medium of variable ionic compositon containing L-tyrosine[14C-U] as DA precursor. A superfusion system was used to study both spontaneous and K+-induced release of labeled DA from striatal slices. The addition of APO directly to the normal KRP medium markedly blocked the formation of [14C]DA from [14C]Tyr with an IC50 [median inhibitory concentration] of 1.8 .times. 10-7 M. Haloperidol (4 .times. 10-7 M), a known DA antagonist, produced a shift to the right of the concentration-response curve for APO inhibition on DA synthesis, whereas the DA antagonist (+)butaclamol (4 .times. 10-7 M) completely reversed the inhibition caused by APO (2 .times. 10-7 M). DA uptake blockers, such as benztropine (2 .times. 10-6 M) or cocaine (1 .times. 10-5 M), did not affect the ability of APO to inhibit DA synthesis. The .alpha.2-adrenergic agonist clonidine produced only a mild inhibition and the .beta.-adrenergic agonist isoproterenol produced no inhibition of [14C]DA formation. APO was able to inhibit DA formation in the absence of Ca in the incubation medium or in the presence of high external Ca concentrations (4, 8 and 24 mM) which depress the rate of DA synthesis. Incubation conditions that cause an increase of free intraneuronal Ca concentrations, such as Na+-free medium, the presence of ouabain (1 .times. 10-4 M), or K+ depolarization, dramatically abolished or impaired the ability of APO to inhibit DA synthesis in striatal slices. It was not possible to demonstrate any change in spontaneous and K+ (27 mM)-induced release of DA in the presence of APO concentrations that produced a marked inhibition of DA synthesis. Tissue slices can evidently be used as a valuable experimental tool to study the inhibitory effect of APO on DA synthesis; this effect occurs through an interaction of APO with presynaptic DA autoreceptors located in striatal dopaminergic nerve terminals. The results do not correlate with the autoreceptor-mediated inhibition of DA synthesis occurring through regulation of Ca influx into the DA nerve terminals. A sensitivity to high intraneuronal Ca concentration may exist during the events that mediate APO-DA autoreceptor interaction and DA synthesis inhibition. DA-synthesis-modulating autoreceptors apparently do not participate in the modulation of DA release.