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Biomedical subjects

B Kanyicska

Publications and source records attributed to B Kanyicska.

At least 37 records · Page 2Linked to original sources
PubMed1987

Diurnal variation in prolactin, adrenocorticotropin and corticosterone release induced by opiate agonists in intact and adrenalectomized rats.

Diurnal variations of the effectivity of beta-endorphin (beta-End), dynorphin (DYN), Met-enkephalin (Met-Enk), D-Met2-Pro5-enkephalinamide (D-Met-Pro-Enk) and morphine to induce prolactin (PRL) and adrenocorticotropin (ACTH)/corticosterone (CS) release in intact and adrenalectomized rats have been examined. The response to morphine (10 mg/kg s.c.), Met-Enk (200 micrograms/rat i.c.v.) and D-Met-Pro-Enk (0.5 microgram/rat i.c.v.) did not change with different times of the day, while that to beta-End (0.5 microgram/rat i.c.v.), DYN (1 microgram/rat i.c.v.) and U50-488H, a selective kappa agonist (10 mg/kg s.c.), showed a circadian rhythm in stimulating PRL release, with a higher increase in the afternoon (16.00-17.00 h) than in the morning (08.00-09.00 h). In adrenalectomized rats the loss of this circadian rhythm was shown. The CS release evoked by morphine, D-Met-Pro-Enk, Met-Enk and DYN was demonstrable only in the morning when the basal CS level was significantly lower than in the afternoon. The afternoon release of ACTH by morphine was higher than in the morning in adrenalectomized rats. beta-End and U50-488H were equally active in the morning and in the afternoon in increasing CS secretion. The present results suggest that the diurnal rhythm in the response of CS and PRL release to opioids is in relation with the glucocorticoid secretion.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1986

The hypothalamic paraventricular nucleus has a pivotal role in regulation of prolactin release in lactating rats.

The affect of paraventricular nucleus (PVN) lesions on PRL secretory response to suckling was studied in adult female rats. Basal levels of PRL were similar in the control and lesioned groups. Substantial decreases in PRL levels occurred after separation of pups from their mothers in the control as well as lesioned animals. When mothers and pups were reunited, the circulating PRL concentrations of the control groups rose immediately from basal values of 50-100 micrograms/liter to reach peaks of 450-550 micrograms/liter. PVN lesions significantly decreased the suckling-induced rise of PRL levels. Furthermore, PVN lesions abolished the high amplitude, episodic pattern of PRL release in continuously lactating rats. These findings are consistent with the view that PVN neurons produce PRL releasing factor(s), which is (are) required for normal secretory patterns of PRL in lactating rats.

Animals↗
PubMed1986

Separation and suckling-induced changes in serum growth hormone levels of lactating rats and their pups.

The effects of separation and suckling on serum growth hormone (GH) levels of lactating rats and their pups were studied on days 1-3 of lactation. The litter size was adjusted to 8 pups/dam without respect to sex. The separation of pups from their mother for 5 h resulted in significant decrease in GH level in the pups. After 30 or 60 min of suckling the level of GH in serum of the pups reached the values of the control group, i.e. non-separated pups. If the pups were attached to pre-suckled mothers, thus consuming less milk, their serum GH levels increased in a significantly lesser extent. It is concluded that some factor(s) are present in milk which stimulate(s) GH secretion of the pups. Due to episodic secretion, high standard error occurred in every group of mothers studied. Mean GH level of freely behaving lactating rats were rather constant. On the other hand, the 5 h separation period and 30 min of suckling seemed to result in decrease and increase in serum GH values, respectively. By the end of a 60 min suckling period, GH declined to low levels again, hence it is likely that the separation and suckling stimuli synchronized GH-episodes. When the litter was replaced with hungry foster pups at 30 min of suckling, GH-decay by 60 min appeared to be less consequent.

Animals↗
PubMed1986

Data suggesting that milk of early lactation period might be involved in sexual differentiation of rat brain.

The contribution of a hypothetic milk factor in the masculinization process of gonadotropin secretion pattern was investigated using a cross-fostering model. Adult female rats whose nipples had been previously excised were mated. At the time of delivery their pups were given to recipient dams that had given birth one week earlier. Pups remaining with their own (intact) mother served as control group. At the age of 37-39 days (birth = day 0) male rats from the experimental and the control groups were castrated and also control females were ovariectomized. Ten days later gonadectomized animals received ovarian grafts excised from 20-day-old rats. Four and seven days after transplantation the grafts were processed for histology. Corpus luteum formation suggests that male rats nursed by recipient dams did not undergo the masculinization process normally occurring during the first few days of postnatal life. In a separate experiment, male pups nursed by dams being at the early lactation (control) or at the midlactation period were decapitated on postpartum day 1 and serum testosterone levels were measured by RIA. Mean testosterone concentration was almost twice as high in the control group than in pups nursed by recipient dams of the midlactation period. These data suggest that milk of the early lactation period might be necessary for the normal masculinization process of the male rat.

Animals↗
PubMed1984

Effects of beta-adrenergic inhibitors on noradrenaline and adrenaline metabolism in brain regions of the rat.

Chloranolol (5 mg/kg i.p.) retarded the disappearance of noradrenaline induced by the dopamine-beta-hydroxylase (DBH) inhibitor FLA 63, in the hypothalamus, nucleus of the solitary tract (A-2/C-2 area), and lateral reticular nucleus (A-1/C-1 area) regions, while propranolol (20 mg/kg i.p.) was effective only in the hypothalamus and in the lateral reticular nucleus. The DBH inhibitor-caused accumulation of dopamine was also inhibited by chloranolol in the solitary tract nucleus. Chloranolol and propranolol were able to antagonize the fall in adrenaline concentration due to the phenylethanolamine-N-methyltransferase (PNMT) inhibitor, Lilly 87130, only in the region of the solitary tract nucleus. The data suggest that beta-adrenergic inhibitors reduce noradrenaline and adrenaline turnover in the central nervous system, most characteristically in the solitary tract nucleus and that this effect is possibly related to their antihypertensive effectiveness.

Adrenergic beta-Antagonists↗
PubMed1984

Loss of sensitivity to morphine induced by prolonged ACTH treatment.

The effect of long term ACTH treatment on some actions of morphine were studied. The effect of ACTH administration was compared to that induced by acute dexamethasone injection. ACTH caused a delayed inhibition of the morphine induced increase in growth hormone secretion demonstrable 24 hr after the last hormone injection. The morphine induced increase of striatal DOPAC (3,4-dihydroxyphenylacetic acid) content was also inhibited by ACTH treatment, however, neither the analgesia, nor the hypermotility caused by morphine were affected. Dexamethasone did not alter significantly the responsiveness to morphine. It is concluded that the prolonged exposure to ACTH presumably causes a corticosterone-mediated loss of responsiveness of functionally restricted opiate sensitive mechanisms in the central nervous system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Decrease of morphine-induced prolactin release by a procedure causing prolonged stress.

The effects of morphine and fentanyl on plasma prolactin levels in rats have been measured. It was found that a prolonged immobilization stressful procedure for 5 h inhibited the response to morphine and fentanyl to increase prolactin secretion, but did not influence the increase in plasma prolactin caused by haloperidol. The injection of a large dose of cortisol (25 mg/kg, s.c.) also evoked an inhibition of morphine-induced prolactin release. The inhibition was maximal 24 h after the administration of the glucocorticoid. These results indicate that stress may induce prolonged alteration in endogenous opioid-mediated neuromodulation via a prolonged release of glucocorticoids.

Animals↗
PubMed1983

Long-term ACTH induced diminished responsiveness of prolactin secretion to morphine.

The effect of morphine on plasma prolactin level and on dopamine turnover in the median eminence was studied using adult male rats chronically treated with ACTH. It was found that the ACTH pretreatment caused a decrease in the effect of morphine on prolactin secretion and prevented the inhibitory effect of morphine on dopamine turnover measured in the median eminence. The prolonged ACTH administration did not influence the prolactin content of the pituitaries and the in vitro dopamine sensitivity of lactotroph cells. Acute dexamethasone injection did not change the morphine-caused prolactin release. These results suggest that chronic ACTH treatment (possibly via corticosterone hyperproduction) elicits an opiate-tolerance like state of tuberoinfundibular dopaminergic neurons.

Adrenocorticotropic Hormone↗
PubMed1983

Changes in dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in human cerebrospinal fluid after L-dopa and deprenyl administration.

The dopamine (DA) and DOPAC levels were measured in cerebrospinal fluid (CSF) using a radioenzymatic method. The influence of a specific monoamine oxidase B inhibitor (deprenyl) on changes in DA and DOPAC levels was studied in untreated patients or after L-dopa administration. A single dose of deprenyl alone did not change the CSF DA and DOPAC levels, a three days' treatment, however, decreased both the DOPAC and DA concentrations. The acute administration of L-dopa caused an increase in CSF DA and DOPAC levels. The changes were smaller following repeated treatment. Deprenyl diminished the increase in DOPAC level after repeated L-dopa administration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Effects of naloxone and neonatal treatment with monosodium-L-glutamate on growth hormone and prolactin release induced by electrical stimulation of the medial-basal hypothalamus in rats.

The role of nerve cells of the arcuate nucleus and endogenous opioid peptides in the regulation of GH and prolactin secretion has been investigated. Electrical stimulation of the medial-basal hypothalamus (MBH) for 10 min raised plasma levels of both hormones in male rats anaesthetized with pentobarbitone sodium. Plasma hormone levels increased within 5 min after the termination of the stimulus, while no marked changes were found during stimulation. The GH response to the electrical stimulus was substantially reduced in rats with arcuate lesions induced by neonatal treatment with monosodium-L-glutamate (MSG). By contrast, the size of the prolactin response was not altered by MSG treatment. The opiate receptor antagonist naloxone (10 mg/kg, i.v.) failed to influence GH secretion induced by electrical stimulation in either control or MSG-treated animals. The post-stimulus rise of plasma prolactin levels was attenuated by naloxone in control rats, while the same dose of the drug was ineffective in rats which had been exposed to MSG. We conclude that endogenous opioids participate in the increase of prolactin release upon electrical stimulation of the MBH but are not involved in the GH secretory response. Arcuate neurones are important in the maintenance of the GH response to electrical stimulation. By contrast, lesioning of the arcuate nucleus failed to affect the prolactin secretory response elicited by MBH stimulation. However, prolactin release in MSG-treated rats appeared less susceptible to the inhibitory action of naloxone, suggesting a possible supersensitivity towards endogenous opioids.

Animals↗
PubMed1982

Renal excretion of sodium after bilateral renal sympathectomy in the anaesthetized and conscious rat.

1. The effect of bilateral renal denervation on sodium excretion was studied in conscious rats on normal, low and high sodium diet, and in rats recovering from anaesthesia, as well as in anaesthetized rats fed a normal sodium diet. 2. Sodium excretion of bilaterally denervated conscious rats on normal sodium intake and during either 2 weeks of sodium depletion or 6 days of sodium loading was not different from that of controls, despite changes in sodium supply of more than two orders of magnitude. Cortical noradrenaline concentration of control kidneys was 138 +/- 12 ng/g, but was only 7 +/- 3 ng/g (P less than 0 . 001) 6 weeks after denervation. 3. In rats recovering from anaesthesia urine flow, sodium excretion and glomerular filtration rate (G.F.R.) were not affected by denervation. 4. In anaesthetized non-diuretic rats on normal sodium diet chronic bilateral renal denervation increased urine flow and sodium excretion four and five times, respectively, with no changes in G.F.R. 5. Mean arterial blood pressure in bilaterally denervated anaesthetized rats and in those recovering from anaesthesia was decreased by 2 . 7 kPa, P less than 0 . 001 and 1 . 2 kPa, P less than 0 . 05, respectively. 6. The participation of renal nerves in the regulation of sodium excretion in conscious rats seems improbable. The denervation natriuresis in anaesthetized rats can be related to higher pre-denervation renal sympathetic nervous activity due to narcosis and surgical stress.

Anesthesia, General↗
PubMed1982

Neonatal treatment with monosodium-L-glutamate: differential effects on growth hormone and prolactin release induced by morphine.

The aim of this study was to investigate further the possible role of nerve cells of the arcuate nucleus in the regulation of growth hormone (GH) and prolactin (PRL) secretion. Newborn male rats were treated with monosodium-L-glutamate (MSG) (4 g/kg body weight subcutaneously) or NaCl (0.5 g/kg) on alternate days for the first 10 days of life, and were used 8-9 weeks afterwards. beta-Endorphin-like immunoreactivity in the arcuate nucleus decreased by 54% after MSG treatment. The dopamine content of the median eminence was reduced to 55% of that in NaCl-treated litter mates. No significant change of dopamine content was found in the other hypothalamic regions examined. Basal levels of plasma PRL were unaltered. Intravenous injection of morphine to urethane-anesthetized animals was 3 times more potent in stimulating PRL secretion in MSG-treated rats, while it was 2.5 times less potent in releasing GH. These data suggest that lesioning of the arcuate nucleus by MSG treatment damages neurons inhibiting PRL secretion, as well as neurons facilitating GH secretion.

Animals↗
PubMed1982

Distribution of monoamines within the median eminence in rats.

The concentration of dopamine, norepinephrine, epinephrine and serotonin was determined in 6 rostrocaudal segments of the median eminence, 2 segments in the pituitary stalk, in the retrochiasmatic area and the pituitary lobes by radioenzymatic microassay in adult rats. The level of dopamine and norepinephrine was measured separately in the medial and lateral portions of the median eminence. All four amines measured were found unevenly distributed inside the median eminence: 1. the highest dopamine level was detected in the middle-caudal portions of the median eminence and in the rostral parts of the pituitary stalk; 2. high norepinephrine concentration was found in the retrochiasmatic area and this gradually diminished caudalwards; 3. relatively high epinephrine level was present in the rostral median eminence and retrochiasmatic area, but that in the caudal median eminence and pituitary stalk was low; 4. the level of serotonin increased caudalwards and showed a highest value in the caudal portion of the pituitary stalk. Relatively high dopamine and serotonin levels were also detectable in all three pituitary lobes where the concentration of norepinephrine was low and that of epinephrine was undetectable.

Animals↗
PubMed1981

Lack of correlation between hypothalamic serotonin and the ether-induced ACTH secretion in adrenalectomized rats.

The central serotonergic system was manipulated using a serotonin receptor antagonist (cyproheptadine), electrolytic lesioning of the raphe nuclei and neurochemical destruction of the serotonergic terminals in the hypothalamus. The effects of these interventions on ether-induced ACTH secretion were studied in adrenalectomized rats. Serotonin, norepinephrine and dopamine concentrations were measured in the medial basal hypothalamus (MBH) or in individual nuclei of the hypothalamus and of certain midbrain regions. Cyproheptadine pretreatment inhibited ether-induced ACTH hypersecretion in adrenalectomized animals. Neither the electrolytic lesions of the midbrain raphe nuclei, nor the neurotoxic destruction of the hypothalamic serotonergic terminals (by intraventricular administration of 5,6-dihydroxytryptamine) caused any alteration of stimulated ACTH secretion after ether inhalation and/or long-term corticoid deficiency. These results suggest a lack of correlation between the activity of the central serotonergic system and the ACTH releasing effect of ether-stress in adrenalectomized rats.

5,6-Dihydroxytryptamine↗
PubMed1980

Effects of reserpine and antidepressants on dopamine and DOPAC (3,4-dihydroxyphenylacetic acid) concentrations in the striatum, olfactory tubercle and median eminence of rats.

The dopamine, noradrenaline and 3,4-dihydroxyphenylacetic acid (DOPAC) levels of various rat brain areas (median emience, olfactory tubercle, rostral and caudal part of the striatum) were measured. The effects of reserpine and antidepressants: amitriptyline, nomifensine and EGYT 475 (1-benzyl-4-/2'-piridylcarbonyl/piperazine) were investigated. The dopamine content of the median eminence proved to be the most sensitive to the depletory effect of reserpine. Reserpine (1 mg/kg i.p.) caused a decrease of dopamine in the median eminence, in the olfactory tubercle and in the rostral striatum but not in the caudal striatum. Amitriptyline and EGYT 475 antagonized the reserpine-induced dopamine depletion in the olfactory tubercle. In the median eminence amitriptyline attenuated the effect of the depletor while nomifensine augmented it; EGYT 475 was without effect. The antidepressants antagonized the reserpine-induced increase of DOPAC in the rostral part of the striatum.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1980

Noradrenergic innervation of the rat hypothalamus:experimental biochemical and electron microscopic studies.

The concentrations of noradrenaline in individual hypothalamic nuclei and in the median eminence were measured 7-10 days following surgical transections of the lower brain stem or electrolytic lesions of the medullary noradrenaline-containing cell groups. Terminal degeneration in the hypothalamus was studied after the same surgical procedures. Direct, monosynaptic connections between the dorsomedial hypothalamic nucleus and all the noradrenaline-containing cell groups investigated were found. Degenerated synaptic boutons were demonstrated in the median eminence, arcuate, dorsomedial, ventromedial, periventricular and paraventricular nuclei following lesions of the solitary tract and of the lateral reticular nucleus. Biochemical measurements indicate that the pontine-medullary noradrenergic cell groups are the source of hypothalamic norepinephrine. Ascending noradrenergic fibers destined to terminate in the hypothalamus are provided by several cell groups, though the bulk of the NA-fibers seem to originate in the A1-group, in the ventrolateral part of the medullary reticular formation. Most of these fibers join the ventral NA bundle, fewer join the dorsal periventricular tract and several probably also join the dorsal NA bundle. A significant overlap was found in the hypothalamic arborization of the noradrenergic fibers, so that no strict topographical organization seems to be present either in their origin or their termination.

Adrenergic Fibers↗