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S Taleisnik

Publications and source records attributed to S Taleisnik.

At least 19 recordsLinked to original sources
PubMed1997

Dual effect of electrochemical stimulation of the medial preoptic area on the release of LH: possible neurotransmitter involvement.

Electrochemical and electrical stimulation of the medial preoptic area (MPA) was shown to induce release of LH in rats. Owing to differences in cytoarchitecture and neural afferents between the medial (mMPA) and lateral (lMPA) parts of the MPA, we decided to explore whether this difference in organization would distinctly influence the secretion of gonadotropin. Both parts of the MPA were electrochemically stimulated on the day of proestrus in freely behaving rats bearing chronic implanted electrodes. An anodic direct current of 100 microA was delivered for 40 s at 11.00 h and blood samples were obtained every hour until 17.00 h. Serum LH concentrations in rats stimulated in the medial part of the MPA showed a robust rise 1 h after the stimulus was applied and the values remained high up to the end of the bleeding period. All these animals ovulated. An initial rise in serum LH was also seen in rats stimulated in the lMPA but serum values thereafter returned to basal levels, significantly lower than those in the mMPA-stimulated or in control, nonstimulated rats. Only 2 rats showed full ovulation and the others failed to ovulate or had partial ovulation. Injection of the serotonin antagonist, methysergide, did not affect the response of rats stimulated in either the mMPA or lMPA. The GABA antagonist, bicuculline, had no effect on LH release evoked by lMPA stimulation but blocked the release induced by mMPA stimulation. This later blockade was partially reversed by the administration of the opioid receptor antagonist, naloxone, suggesting the existence of GABA facilitatory influences on LH release via inhibition of opioidergic inputs to the GnRH neurons. On the other hand, naloxone administration had no effect on LH release evoked by stimulation of the mMPA but partially reversed the inhibition resulting from stimulating the lMPA. These data indicate that the mMPA and lMPA have opposite effects on LH secretion and provide evidence for the possible neurotransmitters involved.

Animals↗
PubMed1993

Intraventricular injection of agents that enhance cyclic adenosine monophosphate formation leads to inhibition of proestrous luteinizing hormone surge in rats.

The effect of increasing hypothalamic levels of 3',5'-cyclic adenosine monophosphate (cAMP) on the preovulatory surge of luteinizing hormone (LH) and ovulation was studied in cycling rats. Animals hearing chronically implanted guiding cannulae into the third ventricle were injected with agents known to enhance the cellular levels of cAMP. Hourly blood samples from the unanesthetized, unrestrained rats were obtained between 11.00 and 17.00 h through a plastic cannula inserted into the jugular vein. Intraventricular injections of serotonin (7.5 mg/ml; 2 microliters) in the morning of proestrous blocked the preovulatory surge of LH and ovulation. This effect was assigned to an increased neuronal level of cAMP because it was prevented by a serum anti-cAMP. Third-ventricle injections of 2 microliters of forskolin (0.5 mmol/l), guanosine 5'-O-(3-thiotriphosphate)(2 mmol/l) or dibutyryl-cAMP (1 mmol/l) at 11.00 h on the day of proestrus mimicked the inhibitory effect of serotonin on the proestrous release of LH. It is suggested that serotonin inhibits LH surge by acting directly on LH-releasing hormone neurons and/or on neurons that provide inputs to these neurons involving cAMP as a second messenger. Neurons releasing gamma-aminobutyric acid (GABA) may serve as interneurons sensitive to serotonin, as well as to cAMP, inasmuch as the inhibitory effect of forskolin on the release of LH was partially blocked by the GABA antagonists, picrotoxin and bicuculline.

Animals↗
PubMed1992

A cyclic AMP mechanism mediates the serotonin-induced increase in glutamic acid decarboxylase activity in the preoptic area and hypothalamus.

Previous studies have shown that the injection of 5-hydroxytryptamine (5-HT) into the third ventricle of rats on the afternoon of proestrus increases glutamic acid decarboxylase (GAD) activity in the preoptic area and the hypothalamus. In the present report we examine the adenylate cyclase-cyclic AMP (cAMP) system as mediator of that effect. The increase in GAD activity induced by intraventricular injection of 5-HT was completely blocked by injecting an antiserum against cAMP into the third ventricle 30 min earlier, whereas an injection of serum from normal rabbits was ineffective. On the contrary, activation of adenylate cyclase activity by intraventricular injection of forskolin increased GAD activity, an effect that was also blocked by anti-cAMP serum. Anti-cAMP serum also lowered GAD activity in the preoptic area and hypothalamus when injected on the morning of proestrus but not when injected in the afternoon, when the values of GAD activity were already low. The results suggest that a cAMP mechanism may be involved in the changes in preoptic-area and hypothalamic GAD activity such as the rise in enzyme activity induced by intraventricular injection of 5-HT.

Animals↗
PubMed1992

Daily variations in the sensitivity of proestrous LH surge in the inhibitory effect of intraventricular injection of 5-HT or GABA in rats.

Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed. In rats acclimated to a 14-h:10-h light:dark cycle the potency of 5-HT to inhibit the LH surge and ovulation was 2.06 and 2.3 times greater, respectively, when injected at 11:00 h than at 13:00 h. Also stimulation of the median raphe nucleus at 11:00 h was significantly more effective in inhibiting these parameters than stimulation at 13:00 h. Similarly, the ability of gamma-amino-butyric acid (GABA) to inhibit the preovulatory LH surge and ovulation was greater in rats injected in the morning than in the afternoon. The results of this study indicate that during proestrus the sensitivity of 5-HT and GABA to induce inhibition of preovulatory LH release and ovulation shows daily variations with maximal effect before the critical period.

Animals↗
PubMed1992

Norepinephrine--stimulated activity of hypothalamic adenylate cyclase varies throughout the estrous cycle of the female rat.

The activity of hypothalamic adenylate cyclase was studied throughout the estrous cycle of the female rat. The activity of the enzyme was determined in particulate fractions obtained from hypothalami of rats killed at 10.00 h and 16.00 h of the 4-day estrous cycle. The activity was assayed in the presence of norepinephrine (10(-8) to 10(-3) M) by the capacity to produce adenosine 3',5' cyclic monophosphate. The basal activity of adenylate cyclase was higher in the morning of estrus than at any other time during the cycle. Norepinephrine-stimulated adenylate cyclase activity, as assessed by the apparent affinity (Kd) and apparent maximum effect, varied during the cycle, showing highest affinity, lowest Kd, in the afternoon of proestrus. The highest level of apparent maximum effect was also found in the afternoon of proestrus declining on diestrous day 2, diestrous day 1 and estrus. The norepinephrine stimulated activity was significantly inhibited by phenoxybenzamine, an alpha-blocker, in the morning of diestrus day 1, whereas on the day of diestrus day 2 and proestrus it was inhibited by the beta-adrenoblocker, propranolol. A similar degree of inhibition by alpha- and beta-blockers was observed in the morning of estrus. These results indicate that the hypothalamic adenylate cyclase coupled to adrenergic receptors shows dynamic changes throughout the estrous cycle.

Adenylyl Cyclases↗
PubMed1991

Glutamic acid decarboxylase activity of the preoptic area and hypothalamus is influenced by the serotonergic system.

The effect of the serotonergic system on glutamic acid decarboxylase (GAD) activity of the preoptic area and the hypothalamus was studied in female rats on the day of proestrus. A circadian rhythm of GAD activity was observed with higher values in rats killed at 1130 h than in rats killed at 1500 h. In rats bearing lesions of the median raphe nucleus (MRn), a nucleus that sends 5-hydroxytryptamine nerve terminals to the areas under study decreased GAD activity. On the contrary, electrochemical stimulation of the MRn enhanced GAD activity in intact rats killed at 1500 h, but not in those killed at 1130 h, an effect that was prevented by the injection of the 5-hydroxytryptamine antagonist, methysergide. Furthermore, the injection of 5-hydroxytryptamine into the third ventricle, either in intact rats in the afternoon or in MRn-lesioned rats in the morning, also increased GAD activity. The results of the present study suggest that activation of the serotonergic system increases GAD activity in the preoptic area and hypothalamus.

Animals↗
PubMed1990

Further evidence of an opposite effect of dorsal and median raphe nuclei on the proestrous surge of LH.

The effect of stimulation or lesions of either the dorsal or the median raphe nucleus on the proestrous surge of LH and on ovulation was studied in rats kept under constant illumination. Electrochemical stimulation (anodic DC of 100 microA during 30 sec) was applied at noon on the day of proestrus through chronically implanted electrodes. Lesions of the raphe nuclei were made by passing a cathodic current of 1 mA for 20 sec through nichrome electrodes stereotaxically implanted. Blood samples from freely behaving rats were obtained hourly through cannulae inserted into the jugular vein. Rats under constant light from diestrous day 1 or diestrous day 2 showed a delay in the onset of the LH surge of the next proestrus. Stimulation applied into the median raphe nucleus inhibited proestrous LH release and blocked ovulation, whereas stimulation of the dorsal raphe nucleus resulted in enhanced LH release in rats under constant light from diestrous day 2 but not from diestrous day 1. In turn, in rats bearing lesions in the dorsal raphe nucleus LH surges were decreased and ovulation was blocked, but rats with lesions in the median raphe nucleus exhibited enhanced LH release. It is concluded that the dorsal and the median raphe nuclei exert opposite effects on the proestrous surge of LH and on ovulation.

Animals↗
PubMed1989

Hypothalamic cyclic AMP after the injection of ovarian steroids into ovariectomized rats.

The effect of ovarian steroids on the concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the hypothalamus was studied in ovariectomized rats. Ovariectomized rats exhibited a lower cAMP concentration than intact rats. The administration of a single dose of estradiol benzoate (50 micrograms/kg body weight) resulted 3 days later in a rise of cAMP values, but levels did not reach those observed in estrous rats. Progesterone (2 mg/rat) injected 3 days after the priming dose of estradiol benzoate produced 4 h later no further changes in hypothalamic cAMP. The changes in hypothalamic cAMP concentration induced by estrogen treatment depend, at least in part, on noradrenergic inputs, since they were prevented by the injection of the norepinephrine synthesis inhibitor, diethyldithiocarbamate. In addition, administration of the beta-blocking agent, propranolol, to estradiol- and estradiol-progesterone-treated rats lowered the concentration of cAMP in the hypothalamus in a dose-dependent manner. In contrast, the administration of an alpha-blocking agent, phenoxybenzamine, had no effect at the tested concentration. The results of this study indicate that estrogen increases cAMP concentration in the hypothalamus by a noradrenergic mechanism involving beta-receptors. Moreover, the findings suggest that estrogen induces an increase in the number of beta-receptor sites, whereas progesterone increases the apparent propranolol sensitivity for these receptor sites.

Animals↗
PubMed1989

Inhibition of proestrous LH surge and ovulation in rats evoked by stimulation of the medial raphe nucleus involves a GABA-mediated mechanism.

The neurotransmitters involved in the inhibition of luteinizing hormone (LH) release induced by electrochemical stimulation (anodic d.c., 100 microA/30 s) of the medial raphe nucleus (MRn) were studied. Stimulation applied at noon on the day of proestrus blocked the preovulatory surge of LH and ovulation. This effect was prevented by pretreating the animals (15 min before stimulation) with the 5-HT antagonist, methysergide (3.5 mg/kg, i.p.). The inhibition of LH release induced by stimulation of the MRn was also suppressed by the injection of the gamma-aminobutyric acid (GABA) antagonists, picrotoxin (0.8 mg/kg, i.p.) and bicuculline (6 mg/kg, i.p.). Injection of 5-HT (15 micrograms) into the third ventricle on the day of proestrus mimicked the effect of MRn stimulation, a response which was prevented by methysergide, picrotoxin or bicuculline. An intraventricular injection of GABA (10 micrograms) also inhibited the preovulatory surge of LH and ovulation, but whereas the administration of bicuculline prevented the effect of GABA, that of methysergide failed to produce any change. It is concluded that stimulation of the MRn inhibits the proestrous surge of LH by activating a serotonergic pathway and that the effect is mediated by GABAergic neurons.

Animals↗
PubMed1988

The inhibition of proestrous LH surge and ovulation in rats bearing lesions of the dorsal raphe nucleus is mediated by the locus coeruleus.

Lesions of the dorsal raphe nucleus (DRn) were shown to block the proestrous surge of LH and the shed of ova normally found the following morning. The possibility that this effect could be mediated by the locus coeruleus (LC) was studied in the present work in view of the fact that stimulation of the LC produced similar responses on LH release and that systemic injection of the beta-adrenergic blocking agent, propranolol, partially prevented the effect of DRn lesions. The blocking effect of DRn lesions on proestrous LH surge and ovulation was reproduced by the injection of either methysergide (1 microgram on the day of proestrus), a serotonin (5-HT) blocking agent, or p-chlorophenylalanine (0.5 microgram on diestrus 1 and diestrus 2), an inhibitor of 5-HT synthesis, into the LC of normal cycling rats. On the contrary, the injection of 5-HT (1 microgram on the day of proestrus) into the LC of rats bearing DRn lesions restored the normal LH surge and ovulation. It is concluded that serotonergic afferents into the LC from the DRn tonically inhibit the activity of LC neurons and that the interference of this inflow results in an activation of neurons and thereby in inhibition of LH release.

Animals↗
PubMed1986

Activation of the CNS noradrenergic system may inhibit as well as facilitate pituitary luteinizing hormone release.

Earlier work established that neural secretion of luteinizing hormone-releasing hormone (LH-RH) and the resultant release of pituitary gonadotropins could be facilitated by activating alpha-receptors of a central noradrenergic (NA) system. The present study emphasizes that central NA mechanisms may also inhibit LH release largely through activation of beta-adrenergic receptors.

Animals↗
PubMed1985

Changes of the release of luteinizing hormone (LH) on the day of proestrus after lesions or stimulation of the raphe nuclei in rats.

The effect of stimulation or lesion of the raphe nuclei on ovulation and on the release of luteinizing hormone (LH) on the day of proestrus was studied in unanesthetized, unrestrained rats. Electrochemical stimulation (anodic DC or 100 microA during 30 s) was applied at 12.00 h on the day of proestrus through chronically implanted stainless steel electrodes. Lesions were made by passing a cathodic current of 1 mA for 20 s through nichrome electrodes stereotaxically implanted and the rats were used 15-30 days later. Blood samples were obtained hourly from the freely behaving rats through a plastic cannula inserted into the external jugular vein. Stimulation in the medial raphe nucleus (MRn) resulted in blockade of ovulation and of the preovulatory LH release. On the contrary, no change of the normal pattern of LH surge nor in the number of ovulating rats was seen after stimulation of the dorsal raphe nucleus (DRn) or in rats stimulated in the mesencephalon outside these nuclei. Injection of p-chlorophenylalanine (PCPA) into the MRn to block 5-hydroxytryptamine (5-HT) synthesis, prevented the effect of MRn stimulation, whereas injection of saline solution did not. Rats bearing lesions destroying the DRn showed decreased proestrous LH surge and blockade of ovulation whereas those with lesions of MRn ovulated normally. Rats with transverse cuts placed just behind the DRn exhibited normal LH release indicating that the effects of destroying the DRn is not due to the interruption of ascending fibers crossing the nucleus. Injections of PCPA in the DRn but not saline solution mimicked the effect of lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Ventral premammillary nuclei mediate pheromonal-induced LH release stimuli in the rat.

The rise in the concentration of LH in the serum that takes place in ovariectomized, estrogen-primed rats exposed to the odors from a cage with bedding soiled by a male rat was completely prevented by bilateral lesions destroying the ventral premammillary (PMv) nuclei. These results suggest that the pheromonal stimuli generate stimuli that course through a pathway which involves the PMv nuclei before they reach the hypothalamus. In addition, the chemosensory information is apparently transmitted centrally by an uncrossed pathway in view of the fact that removal of one vomeronasal organ combined with lesions of the contralateral PMv nucleus, but not of the ipsilateral nucleus, suppressed the release of LH in rats exposed to male odors. Since pheromonal stimuli are known to activate the accessory olfactory system, of which the medial (Me) amygdaloid nucleus and the bed nucleus of the stria terminalis (BNST) are parts, the effect of stimulating these nuclei in rats bearing lesions of the PMv nucleus was also investigated. Unilateral lesions of the PMv nucleus prevented the release of LH in ovariectomized, estrogen-primed rats and the advancement of LH surge in proestrous rats induced by electrochemical stimulation (anodic d.c. 100 microA/30 s) of the ipsilateral Me amygdaloid nucleus but not those induced by stimulation of the contralateral Me amygdaloid nucleus. Similar results were obtained stimulating the medial part of the BNST in proestrous rats. It is concluded that the impulses evoked by pheromonal stimuli inducing LH release in the rat are conveyed by an uncrossed pathway and relay in the PMv nucleus before they reach the medial basal hypothalamus.

Amygdala↗
PubMed1984

Blockade of the release of LH induced by pharmacological suppression of adrenergic inflow into the locus coeruleus.

Previous studies have indicated that stimulation of the locus coeruleus (LC) produced inhibition of the release of LH induced by stimulation of the medial preoptic area (mPOA) in ovariectomized, estrogen-primed rats. A similar response following the application of drugs into the LC was taken as an index of activation of the LC neurons. The injection of the phenylethanolamine N-methyltransferase (PNMT) blocking-agent, 2,3- dichloromethylbenzylamine ( DCMB , 0.5 micrograms) into the LC, 2 and 1 h before starting the mPOA stimulation greatly attenuated the induced release of LH. Injection of saline had no effect. The reduced release of LH in DCMB -treated rats was restored to normal by injecting clonidine (0.5 micrograms) into the LC immediately before the mPOA stimulus started, but not by injecting phenylephrine (0.5 micrograms) or saline (0.5 microliter). The release of LH induced by mPOA stimulation was also blocked in rats in which the alpha 2-antagonist, piperoxane (0.5 micrograms) was injected into the LC but not in those injected with the alpha 1-antagonist, phenoxybenzamine (0.5 micrograms) or the beta-antagonist, propranolol (0.5 micrograms). It is concluded that adrenergic afferents into the LC tonically inhibited the activity of LC neurons and that this effect is mediated by alpha 2-adrenoceptors. Interference with the synthesis of epinephrine or blockade of alpha 2-adrenoceptors resulted in activation of LC neurons and thereby in inhibition of LH release.

Animals↗
PubMed1984

Beta-adrenergic receptors in the premammillary nucleus mediate the inhibition of LH release evoked by locus ceruleus stimulation.

The neurotransmitter and andrenoceptors involved in the inhibition of luteinizing hormone (LH) release induced by stimulating the locus ceruleus nucleus (LC) have been characterized in ovariectomized, estrogen-primed rats in which the release of LH was triggered by electrical stimulation of the medial preoptic area. Blockade of norepinephrine synthesis by the injection of the dopamine beta-hydroxylase inhibitors, diethyldithiocarbamate or fusaric acid, prevented the inhibition of LH release, whereas blockade of epinephrine synthesis by injecting the phenylethanolamine N-methyltransferase inhibitor, 2,3-dichloro-methylbenzylamine, had no effect. In addition, the inhibition of LH release was prevented by systemic injection of propranolol but not of phenoxybenzamine. This inhibition was also suppressed in rats in which the ventral premammillary (PM) nucleus ipsilateral to the stimulated LC was lesioned, or in animals with a transverse cut placed just in front of the PM. A similar response was seen in rats in which propranolol but not phenoxybenzamine was applied to the PM ipsilateral to the stimulated LC. The present results indicate that norepinephrine, acting through beta-adrenoceptors mediates the transmission of impulses which, originating in the LC, inhibit the release of LH. The LC adrenergic fibers synapse in the PM before the neural information they convey is transfered to the gonadotropin-releasing hormone containing neurons.

Animals↗
PubMed1984

Inhibitory influence of the nuclei of the posterior hypothalamus on the pro-oestrous surge of LH.

The effect of transecting caudal afferents to the medial basal hypothalamus on the pro-oestrous surge of LH was studied in cyclic female rats. Rats with transverse cuts placed just in front of the mammillary bodies and caudal to the ventromedial hypothalamic nucleus showed an earlier time of onset of pro-oestrous surge of LH. Conversely, rats with transverse cuts placed 2 mm more caudally or with cuts along the lateral edges of the hypothalamus showed no altered release of LH. Advanced release of LH occurred also in rats in which the ventral premammillary nuclei or the posterior hypothalamic nuclei were bilaterally destroyed but not in those sham operated or with lesions in the dorsal premammillary nuclei. The number of ova ovulated was higher in rats bearing lesions of any of these nuclei but enhanced LH release was seen only in animals with lesions of the posterior hypothalamic nuclei. Electrochemical stimulation (anodic d.c., 100 microA, 15 s) applied at noon of pro-oestrus to the ventral premammillary nucleus, dorsal premammillary nucleus or posterior hypothalamic nucleus prevented ovulation and the preovulatory discharge of LH. It is concluded that inputs from nuclei of the posterior hypothalamus are inhibitory for LH release and could participate in determining the timing and magnitude of the pro-oestrous surge of the hormone.

Afferent Pathways↗
PubMed1983

Hypothalamic cyclic-AMP throughout the 4-day estrous cycle of the female rat.

The concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the hypothalamus was measured in the morning (10.00 h) and in the afternoon (16.00 h) during the 4-day estrous cycle of the female rat. The values were found to rise from the lowest levels on the afternoon of diestrus 1 to the highest levels on the morning of proestrus to decline thereafter. A second less marked peak was seen on the morning of diestrus 1. In rats treated with diethyldithiocarbamate to block norepinephrine (NE) synthesis, the concentration of the nucleotide decreased and remained at steady levels indicating that cyclic variations of cAMP in the hypothalamus are related to the endogenous release of NE. Blocking alpha-adrenergic receptors with phenoxybenzamine or beta-adrenergic receptors with propranolol also resulted in a drop of the concentration of cAMP in the hypothalamus. The effect of phenoxybenzamine was almost constant during the different days of the cycle whereas that of propranolol varied showing maximal effects on diestrus 2 and proestrus and minimal on estrus and diestrus 1. These results suggests that the response of endogenously released NE in the hypothalamus mediated through beta-adrenergic receptors undergo variations during the estrous cycle, whereas those mediated through alpha-adrenergic receptors remain at constant levels.

Animals↗