PubMed Health⌕ Search

Biomedical subjects

S Taleisnik

Publications and source records attributed to S Taleisnik.

At least 37 records · Page 2Linked to original sources
PubMed1983

Release of LH in the female rat by olfactory stimuli. Effect of the removal of the vomeronasal organs or lesioning of the accessory olfactory bulbs.

The release of LH in ovariectomized, estrogen-primed rats exposed to male or female rats was studied. The concentration of LH in the serum was measured in blood samples obtained by an indwelling jugular cannula. A blood sample was taken at 12.00 h and then every hour up to 18.00 h following exposure to another rat on the opposite side of a double wire mesh screen. LH in the serum of control non-exposed rats showed a small rise between 16.00 and 18.00 h as compared to earlier values. Rats exposed to intact or castrated male rats exhibited an enhanced release. Exposure to ovariectomized rats failed to induce any change in the release of LH but exposure to ovariectomized, estrogen-primed rats produced a significant increase. No effect on LH release was seen in animals exposed to a female diestrous rat or to a pregnant rat. Rats exposed to an empty cage which had been soiled by housing a male rat for 3 days, showed an enhanced release of LH similar to those exposed to a cage containing the male rat, indicating the importance of olfactory stimuli in the response. Ovariectomized rats whose vomeronasal organs had been removed or whose accessory olfactory bulbs were lesioned, failed to show any effect on the release of LH when exposed to a male rat. It is concluded that olfactory stimuli arising from male or female rats are capable of modulating the release of LH in female rats and that perception of these stimuli involves the vomeronasal organ-accessory olfactory bulb system.

Animals↗
PubMed1983

Prolactin release induced by stress and the influence of oestrogen and progesterone treatments, sex and daily rhythm.

The effect of sex, ovarian steroids and time of the day on the release of prolactin induced by stress was studied. Albino rats were bled by heart puncture and immediately anaesthetized with ether; 10 min later they were bled again. Ovariectomized, oestrogen-primed rats showed a daily rhythm in the stress (bleeding plus ether) induced prolactin release with maximal concentration of prolactin in the serum at night (01.00 h) and minimum in the morning (09.00 h). IN ovariectomized, oestrogen-treated rats the rise of prolactin in the serum after stress was higher than in the non-treated rats both in the morning and at night. However in the afternoon (17.00 h), when the pre-stress levels of prolactin were high, the response to stress was reversed and prolactin levels declined. A similar effect was seen in the ovariectomized, oestrogen-primed rats 4 h after the injection of progesterone. In these animals the concentration of prolactin in serum was high and declined after stress. However 28 h after injection of progesterone stress failed to induce any change in prolactin release. Progesterone injected into ovariectomized, non-primed rats did not influence the response to stress. In male rats, both intact and castrated, the increase of prolactin concentration in serum after stress was lower than in females and failed to exhibit a circadian rhythm. These results show the importance of the hormonal background and the time of the day in the magnitude of prolactin release induced by stress.

Animals↗
PubMed1982

Dissociation of the inhibitory and facilitatory effects of norepinephrine on the release of LH by premammillary lesions.

A dual action of the adrenergic system on the release of LH has been demonstrated: facilitation mediated by alpha-adrenergic receptors and inhibition mediated by beta-adrenergic receptors. These two actions can be dissociated either by treatment with agents which block-specific adrenergic receptors or by cuts placed just in front of the mammillary bodies (PM cuts) interrupting caudal afferents to the medial basal hypothalamus. These cuts affected the release of luteinizing hormone (LH) in a way similar to that of treatment with the beta-adrenoblocker, propranolol. Thus, in animals with PM cuts (1) the release of LH following the injection of norepinephrine into the third ventricle was enhanced and (2) the blocking action of intraventricular injection of isoproterenol on the release of LH was suppressed whereas the facilitatory effect of clonidine was not changed. Furthermore, whereas the release of LH induced by intraventricular injection of norepinephrine in intact rats was enhanced by treatment with propranolol, in rats with PM cuts the already enhanced induced release was no further raised by propranolol treatment. On the other hand, PM cuts did not affect the suppressive action of the alpha-adrenoblocker phenoxybenzamine on the norepinephrine-induced release of LH. It is concluded that adrenergic mechanisms inhibiting the release of LH were suppressed by PM cuts whereas those facilitating the release were not affected by these cuts.

Animals↗
PubMed1981

Pathways by which stimuli originating in the cingulate cortex inhibiting LH secretion reach the hypothalamus.

The effect of transecting the frontal, lateral, dorsal or caudal afferents to the mediobasal hypothalamus (MBH) on the inhibition of LH release induced by electrochemical stimulation of the anterior cingulate area was studied. Electrochemical stimulation (100 microA/30 s) of the anterior cingulate area applied in ovariectomized estrogen-primed rats immediately after the first 15 min of electrical stimulation in the medial preoptic area (mPOA; monophasic square pulses of 1 ms duration, 50 Hz, 150 microA, 15 s on and 15 s off for 30 min) suppressed the rise in LH observed in control rats 15 min later. This inhibitory effect was prevented either by bilateral parallel cuts along the lateral hypothalamic area (LHA) or by cuts in the premammillary area (PMA) interrupting the caudal afferents to the MBH, whereas it was not affected by suprachiasmatic or periventricular cuts or by transection of the medial corticohypothalamic tract. Unilateral cuts in the LHA also suppressed the effect of anterior cingulate area stimulation when the cortex of the frontal lobe ipsilateral to the side of the lesion was stimulated. None of these lesions interfered with the release of LH triggered by stimulation of the mPOA. Lesions in the LHA or PMA also prevented the blockade of ovulation and discharge of LH on the day of Proestrus induced by electrochemical stimulation of the anterior cingulate area. Besides, electrolytic lesions of the ascending noradrenergic pathways at the level of the dorsal noradrenergic tract or the medial forebrain bundle but not of the locus ceruleus or the A5 cell grouping also suppressed the inhibition of LH secretion. These results indicate that the impulses originated in the anterior cingulate area inhibiting LH release reached the hypothalamus by way of its lateral and caudal aspects and that an adrenergic mechanism is associated with this effect.

Animals↗
PubMed1980

Blockade of ovulation and release of LH in the rat by electrochemical stimulation of the frontal lobe cortex.

The effect of stimulation of the frontal lobe cortex on the release of luteinizing hormone (LH) and ovulation was studied in female rats. Electrochemical stimulation (anodic DC) was applied through monopolar stainless-steel electrodes chronically implanted in the non-anesthetized freely-behaving animals bearing a plastic cannula inserted into the jugular vein for blood sampling. In rats, on the day of proestrus, stimulation (100 uA/30 sec) of the medial cortical surface in the superficial and deep layers of the medial precentral area and of the anterior cingulate area blocked ovulation in about 80% of the animals. A similar effect was seen when the stimulus was applied in the deep layers of the prelimbic and infralimbic areas. On the contrary, stimulation in the superficial layers of these latter two areas, as well as in the superficial and deep layers of the retrosplenial cortex, did not affect normal ovulation. The preovulatory discharge of LH was blocked in the animals which failed to ovulate. The degree of inhibition exerted by the anterior cingulate area and the prelimbic area on ovulation and LH surge was proportional to the amount of current applied. Stimulation of the anterior cingulate area also blocked the release of LH induced by the injection of progesterone into ovariectomized estrogen-primed rats. Furthermore, electrochemical stimulation of the anterior cingulate area inhibited the rise of LH in the serum induced by electrical stimulation of the medial preoptic area of ovariectomized estrogen-injected rats, but it failed to affect that resulting from electrical stimulation of the medial basal hypothalamus. On the other hand, stimulation of the lateral cortical surface and the ventral cortex of the frontal lobe on the day of proestrus affected normal ovulation and LH surge only when the stimulus was applied in the agranular insular area which also exhibited an inhibitory action. It is concluded that certain areas of the frontal lobe cortex related to limbic structures exert an inhibitory influence on ovulation and LH secretion.

Animals↗
PubMed1980

Dual action of electrochemical stimulation of the bed nucleus of the stria terminalis on the release of LH.

The effect of stimulation of the bed nucleus of the stria terminalis (BNST) on ovulation and LH release was studied in unanesthetized, freely moving rats. Electrochemical stimulation (anodic d.c., 100 microA/30 sec) was applied at 11.30 h through chronically implanted monopolar, stainless steel electrodes. Serial blood samples were obtained by way of a plastic cannula implanted in the jugular vein. Stimulation on the day of proestrus prevented ovulation and the preovulatory discharge of LH when the stimulus was applied to the lateral part of the BNST but advanced the surge of LH in those rats stimulated in the medial part of the nucleus. In ovariectomized estrogen-primed rats stimulation in the medial part of the BNST produced LH release but no effect was seen when the stimulus was applied in the lateral part. It is concluded that the BNST is part of a dual system with antagonistic effects on LH secretion.

Animals↗
PubMed1980

Inhibition of secretion of luteinizing hormone induced by electrochemical stimulation of the anterior cingulate cortex mediated by a beta-adrenergic mechanism.

Release of LH occurred in ovariectomized, oestrogen-primed rats when the medial preoptic area (mPOA) was electrically stimulated with monophasic square pulses of 1 ms duration (50 Hz, 150 microA, 15 s on and 15 s off for 30 min). Electrochemical stimulation of the anterior cingulate area applied immediately after the first 15 min period of stimulation in the mPOA completely prevented the rise in LH normally observed during the following 15 min. This effect was suppressed either by selective blockade of noradrenaline synthesis with diethyldithiocarbamate, or following systemic or intraventricular injection of the beta-adrenergic blocker, propranolol, whereas it did not change after systemic atropine, pimozide or phenoxybenzamine. Isoprenaline, a beta-adrenergic agonist, injected into the third ventricle of rats stimulated in the mPOA mimicked the effect of the cortical stimulation, this effect was also blocked by propranolol. Intraventricular administration of propranolol or of isoprenaline had no effect on the release of LH induced by the injection of gonadotrophin releasing hormone, showing that their action is not directly on the pituitary gland. Intraventricular injection of noradrenaline, which failed to affect the release of LH induced by stimulation in the mPOA, inhibited this release when animals were pretreated with phenoxybenzamine. On the other hand, the LH-releasing potency of noradrenaline was greatly increased if the beta-receptors were blocked. From these results it may be concluded (1) that inhibition of the secretion of LH evoked by electrochemical stimulation of the anterior cingulate cortex is mediated by an adrenergic mechanism involving a beta-receptor and (2) that noradrenaline exerts an inhibitory effect on the secretion of LH through a beta-receptor in addition to the known facilitatory action through an alpha-receptor.

Animals↗
PubMed1980

Sensory control of the hypothalamus and the neuroendocrine system.

A study was made of the control of the hypothalamus and neuroendocrine complex by the specialized receptors: the eye, the ear and the olfactory complex. The ancient and modern evidence that light, acting on the optic system, can influence hypothalamic, hypophyseal, endocrine reactions was reviewed and the recently acquired evidence that an optic-hypothalamic-autonomic-pineal-hypothalamic circuit exists which controls liberation of "releasing hormones". Evidence was presented to show that the ear and eye, extero-and interoceptive influences affect lactation and oxytocin secretion by action through the hypothalamus. It was also shown that electrochemical stimulation of the olfactory bulbs can affect both sexual behavior and gonadotropin secretion. Finally, it was shown that the olfactory system exerts some control over water intake, sodium appetite and antidiuretic hormone secretion. Progress in a long term cooperative study of the role of exteroceptor control of neuroendocrine functions was reported.

Animals↗
PubMed1979

Dissociation of spontaneous and mating induced ovulation by frontal hypothalamic deafferentations in the rat.

Different types of anterior hypothalamic deafferentations have been used to investigate the nervous pathways involved in spontaneous and mating-induced ovulation in the rat. Knife cuts which circumscribed the suprachiasmatic nuclei on all but their ventral surface and either their rostral or caudal poles prevented spontaneous ovulation, but the rats were sexually receptive (copulation plugs and sperm in the smear), and mating induced ovulation. Similar types of cut extended dorsally so as to sever the continuity between the preoptic area and the mediobasal hypothalamus also prevented spontaneous ovulation, and although these rats were also receptive, mating did not induce ovulation. Two possible explanations are considered: either (i) that difference between the effects of the two types of cut is a direct function of the differing proportions of gonadotrophic hormone-containing axons severed, or (ii) cuts in the region of the suprachiasmatic nuclei specifically impair a mechanism for the maintenance of diurnal rhythms, to which the abnormality in gonadotrophin control is secondary.

Afferent Pathways↗
PubMed1979

Effect of electrochemical stimulation in the olfactory bulbs on the release of gonadotropin hormones in rats.

The olfactory bulbs were electrochemically stimulated in non-anesthetized, freely moving rats, and the ovulatory response and serum luteinizing hormone (LH) levels were studied. The stimulus was applied at 11:30 h through unilateral stainless steel electrodes chronically implanted, and serial blood samples were obtained by way of a plastic cannula located in the jugular vein. Electrochemical stimulation (100 microA/60 sec) of the main olfactory bulbs in the ventral aspect of the superficial layers as well as in its central core, performed on the day of proestrus, prevented the preovulatory discharge of LH and ovulation. Blockade of ovulation also occurred when the stimulus was applied in the lateral or medial parts of the superficial layers. On the other hand stimulation in the dorsal part blocked the preovulatory surge of LH and ovulation in only 50% of the cases. Stimulation applied in the accessory olfactory bulbs failed to interfere with ovulation and LH discharge. Stimulation of ovariectomized estrogen-primed rats applied in superficial layers of the main olfactory bulbs had no significant effect on the release of LH, but when the stimulus was applied in the accessory olfactory bulb a release of LH took place 3-6 h following stimulation. These results indicate that stimulation of the olfactory bulbs produce a dual effect on LH release: while the response of the accessory olfactory bulb is facilitatory in nature, that of the main olfactory bulbs is inhibitory.

Animals↗
PubMed1978

Facilitatory and inhibitory effects of electrochemical stimulation of the amygdala on the release of luteinizing hormone.

The effect of amygdaloid stimulation on the release of luteinizing hormone (LH) was studied in unanesthetized, unrestrained rats. Electrochemical stimulation (anodic D.C.) was applied at 11.30 h through stainless steel electrodes chronically implanted into different amygdaloid nuclei; medial (Men.), cortical (Con.), central (Cn.), or basolateral (Bln.). A plastic cannula inserted into the jugular vein was used for obtaining blood samples at different times of the experimental procedure. In rats on the day of proestrus, stimulation (100 micronA/30 sec) in the Bln. resulted in blockade of spontaneous ovulation and of the preovulatory LH release and that in the Cn. produced a delay in the hormone discharge. On the contrary, stimulation in the Men. was effective in advancing the time of the normal LH surge, while no change of the normal pattern occurred from the Con. Stimulation (100 micronA/60 sec) of ovariectomized estrogen primed rats applied in the Men. or the Con. induced LH release, while that in the Bln. or the Cn. had no effect. The release of LH by Men. stimulation and the blocking effect of Bln. showed a close relationship with the amount of current delivered. Lower thresholds were required for inhibition than for activation. The release of LH induced by stimulation in the Men. of ovariectomized estrogen primed rats occurred at the same time of the day whether the stimulus was applied at 8.30 h, 11.30 h or 14.00 h, indicating a modulatory effect of the amygdala. No changes in serum LH concentration were observed after stimulation of the Men. of castrated estrogen primed male rats or in the Bln. of ovariectomized non-primed rats. The present results indicate that the amygdala exerts a dual effect on the release of LH, the Bln. being inhibitory and the Men. and Con. facilitatory.

Amygdala↗
PubMed1978

Stimulatory and inhibitory effects of ovarian steroids on gonadotrophin secretion in ovariectomized rats after anterior hypothalamic deafferentation.

The effect of frontal hypothalamic deafferentation on the release of LH and FSH was studied in ovariectomized rats. Frontal cuts were placed just in front of the arcuate nucleus, at the posterior border of the optic chiasma (RCS), at the level of the anterior commissure (POS) and in front of the optic chiasma (PCS). Animals with RCS and POS cuts showed vaginal smears with persistent cornification; the other groups had irregular cycles. The concentrations of LH and FSH in the serum increased after ovariectomy in deafferentated animals, but after 4 weeks the levels were lower than in the animals without hypothalamic lesions except for the PCS group. The more caudally that the cuts were located, the lower were the concentrations of hormones in the serum. The injection of repeated doses of oestradiol benzoate resulted in a decrease in serum gonadotrophin of both rats without hypothalamic lesions and RCS rats. Although a greater decrease was observed in the lesioned than in the intact rats, it is believed that such an effect does not indicate an increased sensitivity of deafferentated animals to this steroid. The stimulatory effect of progesterone on LH and FSH release was studied in ovariectomized rats primed with oestradiol benzoate. The responses were unchanged in PCS animals but failed to occur in POS and RCS rats. Measurement of the level of gonadotrophin-releasing hormone in frontal hypothalamic slices from RCS animals showed a decreased level behind the cut and an increased one in front of it, suggesting that perikarya located in front of the section were sending their axons to the mediobasal hypothalamus. It is believed that the blockade of the stimulatory effect on gonadotrophins by frontal hypothalamic deafferentation is due to the transection of these axons. Cuts placed immediately in front of the arcuate nucleus, however, permitted progesterone-induced gonadotrophin release because of incoming neurones containing gonadotrophin-releasing hormone, which end in structures immediately rostral to the cut. The results indicate that effects of both inhibitory and stimulatory ovarian steroid feedback are impaired by frontal hypothalamic deafferentation.

Afferent Pathways↗
PubMed1977

Further evidence on the role of the hypothalamic afferents on the estrogen-induced prolactin release.

Serum prolactin (Prl) concentrations in ovariectomized rats were low without significant differences between morning and afternoon values. These levels were not affected by either frontal or caudal hypothalamic deafferentation. However, they increased after lesioning the hypothalamic median eminence (ME). Three days after the injection of 20 microgram estradiol benzoate (EB) into ovariectomized non-lesioned rats, a rise in serum Prl occurred in the afternoon but not in the morning. In animals with ME lesions estrogen enhanced both morning and afternoon values. The animals with caudal hypothalamic deafferentation and those which had undergone sham operation showed the same pattern as the normal animals. On the contrary, after estrogen treatment of rats with frontal hypothalamic deafferentation high serum Prl concentration during the morning and low levels in the afternoon were observed. It is concluded that estrogen effects on Prl secretion are in part mediated by frontal neural afferents to the hypothalamus. They would facilitate Prl inhibiting factor (PIF) secretion in the morning and inhibit PIF secretion in the afternoon.

Afferent Pathways↗
PubMed1977

Influence of oestrogen administration in vivo and in vitro on the release and synthesis of prolactin from incubated pituitaries.

The release and synthesis of prolactin were studied in incubated adenohypophyses from ovariectomized rats. After a 4 h incubation period the prolactin concentration in the medium markedly increased whereas that in the gland was reduced. However, the concentration of prolactin in the system, tissue plus medium, after 4 h was almost twice as much as that present at the beginning of incubation indicating spontaneous synthesis. This spontaneous release and synthesis of prolactin was greatly increased in incubated glands from ovariectomized oestrogen-treated rats. Oestradiol benzoate was injected in doses of 2.5, 5.0 or 10.0 microgram/rat 2 or 24 h before killing the animals. Lower effects were obtained in glands from 2 h-oestradiol-pre-treated rats than from 24 h-oestradiol-primed rats. Oestradiol-17beta (55, 166, 500 and 1500 ng/ml) added to the incubation medium also enhanced the release and synthesis of prolactin and the effect was more marked in glands from oestrogen injected rats than in those of non-treated animals. The increase was dose-related although the higher doses were less effective. These results provide further evidence of the effect of oestrogen on the release and synthesis of prolactin by a direct action on the pituitary gland. They also show that oestradiol pre-treatment in vivo increase the response of the prolactin cells towards oestradiol in vitro.

Animals↗
PubMed1976

The role of hypothalamic afferents in the release of prolactin induced by ovarian steroids.

The importance of frontal and caudal afferents to the hypothalamus in the release of prolactin induced by estrogen and progesterone was studied in gonadectomized female and male rats. The serum prolactin levels 2 or 3 days after the injection of 20 mug estradiol benzoate (EB) into ovariectomized rats were significantly lower in animals with retrochiasmatic section interrupting the anterior inputs to the hypothalamus than in control animals, whereas the prolactin secretion induced by progesterone (2 mg) injection in EB-primed animals was not affected. On the contrary, interruption of caudal afferents to the hypothalamus had no effect on the increase in serum prolactin induced by EB injection. A hypersensitive prolactin response to the injection of estrogen or progesterone occurred in animals with frontal hypothalamic deafferentation. It is concluded that prolactin secretion induced by estrogen injection depends not only on the activation of hypothalamic and pituitary mechanisms, but also on the stimulation of frontal neural afferents to the hypothalamus. The latter mechanism does not operate in male rats.

Animals↗