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K Fink

Publications and source records attributed to K Fink.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Effect of incubation time in deep freezing human sperm].

For the protection of spermatozoa against deleterious influences during freezing and thawing, so-called "cryoprotective agents" are mixed with the ejaculate before freezing. Clinical experience indicated a decrease in the number of post-thaw motile sperms after increasing the incubation period of sperms with the added cryoprotective agents and prompted us to investigate this finding. In experiment 1 we used 21 ejaculates which had a mean motility rate of 63.3%. The ejaculates were divided into 3 portions (1 a, 1 b, 1 c), which were frozen after 10 (1 a), 30 (1 b), and 60 (1 c) minutes of equilibration respectively. After thawing, 18.4% (1 a), 12.8% (1 b), and 7.1% (1 c) of the sperms were motile. This decrease in sperm motility was highly significant (p = 0.0012). Cryosurvival was investigated more fully within the first 10 minutes of incubation in a second experiment with another 18 ejaculates. The ejaculates were divided into 2 portions; portion 2 a was mixed with the cryoprotectant and frozen immediately and portion 2 b was frozen after a 10 minute incubation time. There was no significant difference in post-thaw motility and in recovery rate between the groups 2 a and 2 b. Our results indicate that the cryoprotective agent has a toxic time-dependent negative influence on sperm quality during equilibration, which significantly increases after an incubation time of more than 10 minutes. We consider that the results of this study are applicable to other glycerol-containing cryoprotectants and we recommend that the incubation period is kept short.

Humans↗
PubMed1990

Inhibition of N-methyl-D-aspartate-induced noradrenaline release by alcohols is related to their hydrophobicity.

In rat brain cortex slices, ethanol was three times more potent in inhibiting [3H]noradrenaline ([3H]NA) release evoked by N-methyl-D-aspartate (NMDA) than in inhibiting the release evoked by kainic acid. Methanol, 1-propanol, 1-butanol, 1-pentanol and 1-hexanol shared the inhibitory property of ethanol on NMDA-evoked [3H]NA release. The inhibitory potency of the alcohols, as expressed by their IC50 values, was correlated with their membrane/buffer partition coefficient. It is concluded that the inhibitory effect of the alcohols may be due to a hydrophobic interaction with the NMDA receptor system.

Alcohols↗
PubMed1990

Involvement of presynaptic H3 receptors in the inhibitory effect of histamine on serotonin release in the rat brain cortex.

Rat brain cortex slices or synaptosomes preincubated with 3H-serotonin were superfused with physiological salt solution (which, in the case of slices, contained citalopram, an inhibitor of serotonin uptake), and the effects of histamine and related drugs on the evoked tritium overflow were studied. The electrically (3 Hz) evoked tritium overflow from slices was inhibited by histamine and the H3 receptor agonists R-(-)-alpha-methylhistamine and N alpha-methylhistamine (pIC12.5 values: 6.41, 7.28 and 6.12, respectively), but not affected by the H1 receptor agonist 2-(2-thiazolyl)ethylamine and the H2 receptor agonist dimaprit (each at 10 mumol/l). The concentration-response curve for histamine was shifted to the right by the H3 receptor antagonists impromidine, burimamide and thioperamide (apparent pA2 values: 7.45, 5.97 and 7.88, respectively); the concentration-response curve of serotonin for its inhibitory effect on the electrically evoked overflow was not affected by the three drugs (apparent pA2 values: less than 5.5, less than 5.5 and less than 6.5). Given alone, impromidine, thioperamide and a low concentration of burimamide facilitated the electrically evoked overflow. In slices superfused with K(+)-rich, Ca2(+)-free solution containing tetrodotoxin throughout and in synaptosomes superfused with Ca2(+)-free solution, histamine inhibited the overflow evoked by introduction of Ca2+ (in synaptosomes, simultaneously with an increased amount of K+). In either tissue, the effect of histamine was counteracted by thioperamide. The results provide evidence that exogenous and probably also endogenous histamine inhibits serotonin release in the rat brain cortex via presynaptic histamine H3 receptors.

Animals↗
PubMed1990

Veratridine and other depolarizing agents counteract the inhibitory effect of Mg2+ ions on N-methyl-D-aspartate (NMDA)-induced noradrenaline release in vitro.

Rat brain cortex slices preincubated with 3H-noradrenaline were superfused with Krebs-Henseleit solution with or without Mg2+. In the absence of Mg2+ ions, NMDA evoked 3H-noradrenaline overflow above basal efflux; this effect was concentration-dependently inhibited by Mg2+ (IC50: 19 mumol/l). Despite the presence of 1.2 mmol/l Mg2+, which is known to block cation influx through the ion channel coupled to the NMDA receptor, NMDA evoked 3H-noradrenaline release if the membrane was permanently kept depolarized by 20 or 25 mmol/l K+, 1 mumol/l veratridine or 200 mumol/1 3,4-diaminopyridine; the stimulant effect of NMDA was counteracted by 2-amino-5-phosphonovaleric acid (2-APV), a competitive antagonist at the NMDA receptor and by (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohept-5,10-imine hydrogen maleate (MK 801), an antagonist acting at the cation channel associated with the NMDA receptor. In contrast, no stimulatory effect of NMDA in the presence of 1.2 mmol/l Mg2+ was observed when the membrane of the nerve terminals was intermittently depolarized by electrical impulses of 2 ms duration at a frequency of 1-3 Hz. It is concluded that continuous depolarization of the nerve membrane counteracts the blocking effect of Mg2+ on cation influx through the NMDA receptor-associated ion channel. Under this condition, noradrenaline release can be stimulated by NMDA receptor activation even in the presence of physiological Mg2+ concentrations.

2-Amino-5-phosphonovalerate↗
PubMed1990

Distinction of NPY receptors in vitro and in vivo. I. NPY-(18-36) discriminates NPY receptor subtypes in vitro.

We studied the possibility of multiple neuropeptide Y (NPY) receptor subtypes. NPY-stimulated Ca2+ mobilization in human erythroleukemia (HEL) cells was used to screen a number of NPY analogues. The potencies of three of these analogues [peptide YY (PYY), [D-Tyr-36]NPY, and NPY-(18-36)] were compared with that of NPY in the following model systems: Ca2+ mobilization and inhibition of adenosine 3',5'-cyclic monophosphate accumulation in HEL cells, potentiation of vasoconstriction in the isolated rabbit ear artery, reduction of cutaneous microvascular perfusion in the rat digit, and inhibition of [3H]serotonin release in rat brain. In each of the five models, PYY was a full agonist that exhibited a similar or slightly higher potency than NPY, whereas [D-Tyr-36]NPY and NPY-(18-36) were partial agonists with lower potencies: NPY-(18-36) had a lower potency and efficacy than [D-Tyr-36]NPY in HEL cells and the rabbit ear artery, but was more effective than [D-Tyr-36]NPY for constricting cutaneous microvasculature and inhibiting serotonin release. Because of its weak partial agonism, we also tested NPY-(18-36) as an antagonist of NPY-stimulated Ca2+ mobilization in HEL cells. NPY-(18-36) shifted the NPY concentration-response curve to the right with a KB affinity value of 297 nM. In summary, [D-Tyr-36]NPY and NPY-(18-36) are partial agonists, the relative potency of which varies between systems. These data demonstrate the presence of multiple NPY receptor subtypes. We propose a modified classification scheme of NPY receptor subtypes.

Animals↗
PubMed1989

Inhibition of noradrenaline release in the pig coronary artery via a novel serotonin receptor.

In pig coronary artery preincubated with [3H]noradrenaline, the effects of serotonin (5-HT) receptor agonists and antagonists on the electrically evoked (0.66 Hz) tritium overflow were determined. Tritium overflow was inhibited by 5-HT, 5-aminotryptamine, N,N-dimethyl-5-hydroxytryptamine, 5-hydroxytryptamine, 5-methoxy-3(1,2,3,6-tetrahydropyridin-4-yl)-1H-indole (RU 24969) and tryptamine. The maximum inhibition obtainable with 5-HT was by about 35%, its pIC20 value was 7.85. 8-Hydroxy-di(n-propylamino)tetralin, urapidil, ipsapirone, 5-carboxamidotryptamine, 4-hydroxytryptamine, 5-methoxytryptamine and alpha-methyl-5-hydroxytryptamine did not decrease 3H overflow. The inhibitory effect of 5-HT was not antagonized by ketanserin, mesulergine, metitepine, propranolol, (3 alpha-tropanyl)-1H-indole-3-carboxylic acid ester (ICS 205-930) and yohimbine. Additionally, it was not altered by indomethacin. We conclude from the present data that the sympathetic nerves of the pig coronary artery are endowed with inhibitory presynaptic 5-HT receptors which do not belong to the 5-HT1, 5-HT2 or 5-HT3 receptor type but seem to represent a so far unknown receptor class.

Animals↗
PubMed1989

N-methyl-D-aspartate (NMDA) receptor-mediated stimulation of noradrenaline release, but not release of other neurotransmitters, in the rat brain cortex: receptor location, characterization and desensitization.

Rat brain cortex slices and synaptosomes (in a few experiments also hippocampal synaptosomes) preincubated with 3H-noradrenaline, 3H-5-hydroxytryptamine, 3H-choline, 3H-glutamate or 3H-gamma-aminobutyric acid were used to investigate the 3H-transmitter release in response to exposure to N-methyl-D-aspartate (NMDA) and other excitatory amino acids. The slices and synaptosomes were superfused with Mg2+-free, otherwise physiologically composed salt solution. In cortical slices preincubated with 3H-noradrenaline, NMDA concentration-dependently stimulated 3H overflow, whereas no such effect occurred in slices preincubated with 3H-5-hydroxytryptamine, 3H-choline, 3H-glutamate or 3H-gamma-aminobutyric acid. In cortical slices preincubated with 3H-noradrenaline, the NMDA-evoked 3H overflow was abolished by tetrodotoxin, presence of Mg2+ 1.2 mmol/l or absence of Ca2+. 2-Amino-5-phosphonovaleric acid produced a parallel shift to the right of the NMDA concentration-response curve, whereas (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohept- 5,10-imine hydrogen maleate (MK-801) not only shifted the concentration-response curve to the right but also reduced the maximum effect of NMDA. Other excitatory amino acid receptor agonists also stimulated 3H overflow, yielding the following rank order of potency: NMDA greater than L-glutamate greater than L-aspartate. Kainate and, in particular, quisqualate exhibited only low potencies and/or intrinsic activities. Prolonged (25 min) exposure of 3H-NA-preincubated cortical slices to a high NMDA concentration produced a short-lasting peak of 3H overflow, followed by a second phase lasting as long as the compound was present; in this phase, 3H overflow was clearly less pronounced and gradually decreased with time.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1989

The pharmacological properties of the presynaptic serotonin autoreceptor in the pig brain cortex conform to the 5-HT1D receptor subtype.

The effects of serotonin receptor agonists and antagonists on the electrically (3 Hz) evoked 3H overflow were determined on pig brain cortex slices preincubated with 3H-serotonin and superfused with physiological salt solution containing indalpine (an inhibitor of serotonin uptake) plus phentolamine. The potencies of the serotonin receptor agonists and antagonists were compared with their affinities for 5-HT1A, 5-HT1B, 5-HT1C, and 5-HT1D binding sites in pig or rat tissue membranes; in addition, the potencies of the agonists were compared to their potencies in inhibiting adenylate cyclase activity in membranes of calf substantia nigra. In the superfusion experiments on pig brain cortex slices the following rank orders of potencies were obtained: agonists, serotonin greater than 5-methoxytryptamine = 5-carboxamidotryptamine greater than RU 24969 (5-methoxy-3(1,2,3,6-tetrahydropyridin-4-yl)-1H-indole) greater than SDZ 21009 (4(3-terbutylamino-2-hydroxypropoxy)indol-2-carbonic-acid-isopr opylester) greater than or equal to yohimbine greater than or equal to cyanopindolol greater than 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin) greater than or equal to CGS 12066 B (7-trifluoromethyl-4(4-methyl-1-piperazinyl)-pyrrolo[1,2-a]quinoxaline); ipsapirone and urapidil were ineffective; antagonists (antagonism determined against 5-methoxytryptamine as an agonist), metitepine greater than metergoline greater than mianserin. Propranolol, spiperone or mesulergine did not produce a shift of the concentration-response curve for 5-methoxytryptamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Inhibition of N-methyl-D-aspartate (NMDA)- and L-glutamate-induced noradrenaline and acetylcholine release in the rat brain by ethanol.

The influence of ethanol on stimulation-evoked 3H-transmitter release was examined in slices of the rat brain cortex and corpus striatum preincubated with 3H-noradrenaline and 3H-choline, respectively. 3H-Transmitter release was stimulated by NMDA, L-glutamate, electrical impulses, reintroduction of Ca2+ ions ("Ca2(+)-evoked release", after superfusion with Ca2(+)-free, K(+)-rich solution) or veratridine. In cortical slices preincubated with 3H-noradrenaline and superfused with Mg2(+)-free, otherwise physiologically composed salt solution, ethanol inhibited the NMDA- or L-glutamate-induced tritium overflow (IC50 45 and 37 mmol/l, respectively). In contrast, the tritium overflow in response to electrical stimulation, reintroduction of Ca2+ ions or veratridine was not affected by ethanol at concentrations up to 320 mmol/l; these experiments were carried out in cortical slices superfused with solution containing a physiological Mg2+ concentration. Ethanol also failed to inhibit Ca2(+)-evoked release in the absence of Mg2+ ions. In the presence of 1 mumol/l veratridine, but not in its absence, NMDA induced tritium overflow even when cortical slices were superfused with salt solution containing a physiological Mg2+ concentration; again, ethanol inhibited this NMDA-evoked tritium overflow (IC50 73 mmol/l. In striatal slices preincubated with 3H-choline and superfused with Mg2(+)-free "physiological" salt solution the NMDA-evoked tritium overflow was also, although at lower potency, inhibited by ethanol (IC50 192 mmol/l). In spite of the differences between the IC50 values of ethanol determined for the inhibition of cortical noradrenaline and striatal acetylcholine release, it may be concluded that the NMDA receptor-ion channel complex is one of the sites of action underlying the ethanol-induced inhibition of neurotransmitter release.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

Inhibition of noradrenaline release in the rat brain cortex via presynaptic H3 receptors.

The effects of histamine and related drugs on the evoked tritium overflow from superfused rat brain cortex slices preincubated with 3H-noradrenaline were determined. Tritium overflow was stimulated electrically (3 Hz; slices superfused with normal physiological salt solution) or by introduction of CaCl2 1.3 mmol/l (slices superfused with Ca2(+)-free medium containing K+ 20 mmol/l). Histamine slightly decreased the electrically evoked 3H overflow in slices superfused in the presence of desipramine. The degree of inhibition obtained with histamine was doubled when both desipramine and phentolamine were present in the superfusion medium (pIC15 6.46). Under the latter condition, the evoked overflow was inhibited by the H3 receptor agonist R-(-)-alpha-methylhistamine and its S-(+) enantiomer (pIC15 7.36 and 5.09, respectively), but was not affected by the H2 receptor agonist dimaprit and the H1 receptor agonist 2-thiazolylethylamine (both at up to 32 mumols/l). The concentration-response curve of histamine was shifted to the right by the H3 receptor antagonists thioperamide, impromidine and burimamide (apparent pA2 8.37, 6.86 and 7.05, respectively), by the H2 receptor antagonist ranitidine (apparent pA2 4.27) and was not affected by the H1 receptor antagonist dimetindene (32 mumols/l). The inhibitory effect of R-(-)-alpha-methylhistamine on the evoked overflow was also counteracted by thioperamide. Given alone, none of the five histamine receptor antagonists affected the evoked overflow. In the absence of desipramine plus phentolamine, impromidine and burimamide facilitated the electrically evoked 3H overflow whereas thioperamide had no effect. The facilitatory effects of impromidine and burimamide were abolished by phentolamine, but not affected by desipramine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Steroid action on gene expression: possible roles of regulatory genes and nuclear acceptor sites.

There has been exciting progress in the understanding of the mechanism of action of steroid hormones. The structures and functions of the various receptor protein domains as well as the various domains of steroid-regulated genes, including steroid response elements, are currently being elucidated. The roles of transcription factors in the steroid-altered regulation of gene transcription are just being defined. The nature of the nuclear acceptor sites, i.e. nuclear-binding sites, for steroid receptors are under investigation. The composition, location, and function of these nuclear acceptor sites for steroid receptors is crucial for understanding the mechanism of steroid regulation of gene expression. Possible roles of specific, DNA-binding, chromatin proteins in these acceptor sites have been suggested. A very rapid action of steroids on the expression of proto-oncogenes that code for nuclear regulatory proteins has recently been described. Using this information, we have proposed a novel steroid action model utilizing "regulatory genes" whereby the steroids would rapidly alter the expression of regulatory genes (early genes) whose protein products would return to the nucleus to regulate the expression of structural genes (late genes). The latter would occur via binding of these regulatory proteins (e.g. transcription factors) to the steroid-regulatory elements neighboring these late genes. This model would explain many of the characteristics reported from many laboratories on the action of steroid hormones on gene expression.

Animals↗
PubMed1989

Rapid inhibition of c-myc gene expression by a glucocorticoid in the avian oviduct.

The glucocorticoid dexamethasone (DEX) causes a rapid, reversible reduction in c-myc mRNA level in the oviducts of estrogen-treated, immature chickens. The c-myc mRNA level begins to decrease by 5 min after injection of 0.5 mg DEX, reaches a minimum of 10% of the control value by 30 min, and returns to 30-40% of the control value by 4 h post injection. This rapid effect of DEX on the c-myc mRNA level occurs in both diethylstilbestrol-stimulated and diethylstilbestrol-withdrawn oviducts. The effect is dose dependent, with reduction of the c-myc mRNA measured with as little as 10 micrograms DEX injection (0.03 micrograms/g BW). The effect of the steroid is gene specific with H2B histone mRNA displaying a significantly reduced response. The effect is also tissue specific with liver displaying an increase of 170% of control values in c-myc mRNA level by 30 min after injection of 0.5 mg DEX. The reduction of avian oviduct c-myc mRNA levels by DEX may play a role in glucocorticoid inhibition of cell proliferation in this tissue. The rapidity of the steroid effects on c-myc expression makes it likely that the steroid-induced reduction of c-myc mRNA levels represents a direct primary action of the steroid-receptor complex on the c-myc gene expression.

Animals↗
PubMed1989

From symmetry to asymmetry.

An introduction is given on Matte Blanco's theory about symmetrical and asymmetrical thought processes and their correspondence with primary and secondary thought processes. The system unconscious is seen in terms of Matte Blanco's principles of symmetry and generalization and their implication in the absence of time, space and the differentiation between the whole and its parts. Clinical material from two cases of agoraphobia are shown as examples of a disturbance or absence of the concept of space in the unconscious and its translation into a symptomatology. The result of psychoanalysis of both cases and its implication is discussed.

Adult↗
PubMed1988

Identification of presynaptic 5-HT1 autoreceptors in pig brain cortex synaptosomes and slices.

Pig brain cortex synaptosomes and slices preincubated with 3H-5-hydroxytryptamine (3H-5-HT) were superfused with physiological salt solution containing citalopram (an inhibitor of 5-HT uptake), and the effects of indolethylamines and 5-HT receptor antagonists on the potassium- or electrically evoked 3H overflow were determined. The potassium (25 mmol/l)-evoked tritium overflow from cortex synaptosomes was inhibited by 5-HT; the inhibitory effect of 5-HT was counteracted by metitepine, which, by itself, did not affect the evoked overflow. 5-Methoxytryptamine (examined in the absence of citalopram) also produced an inhibition of the evoked overflow. In cortex slices, the electrically (3 Hz) evoked overflow was inhibited by 5-HT and 5-carboxamidotryptamine. The inhibitory effect of 5-HT was antagonized by metitepine, which, given alone, increased the evoked overflow, but was not attenuated by ketanserin and ICS 205-930 ([3 alpha-tropanyl]-1H-indole-3-carboxylic acid ester), which, by themselves, did not influence the evoked overflow. The present results suggest that the serotoninergic nerve fibres of the pig brain cortex are endowed with presynaptic 5-HT1 receptors, which can be activated by endogenous and exogenous 5-HT.

Animals↗
PubMed1987

Influence of eicosanoids on serotonin release in the rat brain: inhibition by prostaglandins E1 and E2.

Superfused rat brain cortex slices, hypothalamic slices and cortex synaptosomes preincubated with 3H-serotonin or 3H-noradrenaline were used to study the effects of eicosanoids on tritium overflow evoked either electrically (3 Hz; slices) or by potassium 12 mmol/l (synaptosomes). 1. The electrically evoked 3H overflow from cortex slices preincubated with 3H-serotonin was inhibited by prostaglandins E1 and E2 and by the prostacyclin analogue iloprost. No effect was seen with prostaglandin F2 alpha, prostaglandin D2, CG 4203 (another prostacyclin analogue), U 46619 (a thromboxane A2 analogue) and leukotriene C4. The same held true for indomethacin and the prostaglandin receptor antagonists SC 19220 and N-0164. The inhibitory effect of prostaglandin E2 was slightly more pronounced in the presence of indomethacin than in its absence, but was not affected by SC 19220, N-0164 or forskolin plus AH 21-132 (an inhibitor of cAMP phosphodiesterase). Yohimbine and the serotonin receptor antagonist metitepin failed to influence the inhibitory effect of prostaglandin E1. 2. The potassium-evoked 3H overflow from cortex synaptosomes preincubated with 3H-serotonin was inhibited by prostaglandin E2. 3. Prostaglandin E2 also inhibited the electrically evoked 3H overflow from hypothalamic slices preincubated with 3H-serotonin. 4. The electrically evoked 3H overflow from cortex slices preincubated with 3H-noradrenaline was inhibited by prostaglandin E2, but was not affected by SC 19220, which, in turn, did also not alter the effect of prostaglandin E2. The present results are compatible with the view that presynaptic SC 19220-insensitive prostaglandin E receptors may be involved in the inhibitory effect of prostaglandins E1 and E2 on serotonin (and noradrenaline) release.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1987

Inhibition of noradrenaline release via presynaptic 5-HT1B receptors of the rat vena cava.

In the rat inferior vena cava preincubated with 3H-noradrenaline, the effects of nine serotonin (5-HT) receptor agonists and of eight antagonists (including two beta-adrenoceptor blocking agents) on the electrically evoked 3H overflow were determined. 1. 5-HT, 5-carboxamido-tryptamine, 5-methoxy-3(1,2,3,6-tetrahydropyridine-4-yl)-1H-indole (RU 24969), 5-methoxytryptamine, N,N-dimethyl-5HT, tryptamine and 5-aminotryptamine inhibited the evoked 3H overflow. The potencies of these agonists in inhibiting overflow were significantly correlated with their affinities for 5-HT1B binding sites, but not with their affinities for 5-HT1A, 5-HT1C or 5-HT2 binding sites. 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, and ipsapirone, a partial agonist at these receptors, did not inhibit overflow. 2. Cyanopindolol facilitated the evoked 3H overflow, an effect which was abolished by propranolol. The maximum inhibition of overflow obtainable with 5-HT was diminished by cyanopindolol. 3. The concentration-response curve for 5-HT was shifted to the right by metitepine, metergoline, quipazine, 6-chloro-2-(1-piperazinyl)pyrazine (MK 212) and propranolol which, given alone, did not affect 3H overflow. The apparent pA2 values of these antagonists tended to be correlated with their affinities for 5-HT1B (but not 5-HT1A, 5-HT1C or 5-HT2) binding sites. Ketanserin, a 5-HT2 receptor antagonist, and spiperone, which blocks 5-HT2 and 5-HT1A but not 5-HT1B or 5-HT1C receptors, failed to antagonize the effect of 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗