Biomedical subjects

H Vaudry

Publications and source records attributed to H Vaudry.

At least 271 records · Page 15Linked to original sources

PubMed1995

Vasopressin-responsive adrenocortical tumor in a mild Cushing's syndrome: in vivo and in vitro studies.

We report a case of a Cushing's syndrome caused by an autonomously secreting unilateral adrenocortical tumor, characterized by a clinically and biologically mild hypercortisolemic state and an unusual response pattern to vasopressin. Laboratory tests showed normal early morning plasma cortisol and 24-h urinary cortisol excretion, but lack of nycthemeral variations and suppressed plasma ACTH. Urinary cortisol excretion was not suppressed by either the low dose or the high dose dexamethasone test. Injection of lysine vasopressin, (10 IU, im) induced a marked increase in plasma cortisol, without an elevation of plasma ACTH. Computed tomography scan revealed an adrenocortical mass of the left gland with a contralateral atrophic gland. Removal of the tumor led to complete remission of Cushing's symptoms. In vitro studies were then performed to investigate the effect of arginine vasopressin (AVP) on calcium mobilization in cultured tumor cells using a microfluorimetric technique. Application of AVP in the vicinity of the cells induced a rapid and marked increase in the intracellular calcium concentration. Preincubation of the cells with the V1 vasopressin receptor antagonist [d(CH2)5,Tyr(OMe)2]AVP totally suppressed the AVP-induced stimulation of intracellular calcium concentration. Reverse transcription followed by polymerase chain reaction of tumor ribonucleic acid with specific oligonucleotides amplified high levels of V1 receptor signal compared with normal adrenocortical ribonucleic acid. Specific oligonucleotides for the V2 or V3 receptors amplified only a faint signal. This is the first report describing a mild case of Cushing's syndrome caused by an AVP-sensitive cortisol-producing adenoma. The direct effect of AVP on cultured tumor cells was mediated through the V1 type of vasopressin receptor, similar to that previously characterized in normal human fasciculata cells, suggesting that the tumor expressed an eutopic V1 AVP receptor and exhibited overresponsiveness to AVP.

Adrenal Cortex Neoplasms↗

PubMed1995

Mechanism of action of gamma-aminobutyric acid on frog melanotrophs.

We have previously demonstrated that gamma-aminobutyric acid (GABA) is a potent regulator of secretory and electrical activity in melanotrophs of the frog pituitary. The aim of the present study was to investigate the intracellular events which mediate the response of melanotrophs to GABA. We first observed that GABA (1-100 microM) inhibited both basal and forskolin-stimulated cyclic AMP (cAMP) formation. The inhibitory effect of GABA on cAMP levels was mimicked by the GABAB receptor agonist baclofen (100 microM) and totally abolished by a 4-h pretreatment with pertussis toxin (0.1 microgram/ml). In contrast, the specific GABAA agonist 3-aminopropane sulphonic acid (3APS) did not affect cAMP production. Both GABA and 3APS (100 microM each) induced a biphasic effect on alpha-MSH release from perifused frog neurointermediate lobes, i.e. a transient stimulation followed by an inhibition of alpha-MSH secretion. Administration of forskolin (10 microM) prolonged the stimulatory phase and attenuated the inhibitory phase evoked by GABA and 3APS, indicating that cAMP modulates the response of melanotrophs to GABAA agonists. Ejection of 3APS (1 microM) in the vicinity of cultured melanotrophs caused a massive increase in intracellular calcium concentration ([Ca2+]i). The stimulatory effect of 3APS on [Ca2+]i was abolished when the cells were incubated in a chloride-free medium. The formation of inositol trisphosphate was not affected by 3APS, suggesting that the increase in [Ca2+]i cannot be ascribed to mobilization of intracellular calcium stores. omega-Conotoxin did not alter the secretory response of frog neurointermediate lobes to 3APS, while nifedipine blocked the stimulation of alpha-MSH secretion induced by 3APS. In conclusion, the present data indicate that, in frog pituitary melanotrophs, (i) the stimulatory phase evoked by GABAA agonists can be accounted for by an influx of calcium through L-type calcium channels, (ii) the inhibitory effect evoked by GABAB agonists can be ascribed to inhibition of adenylate cyclase activity and (iii) cAMP attenuates the inhibitory phase evoked by GABAA agonists. Taken together, these data suggest that activation of GABAB receptors may modulate GABAA receptor function.

Adenylyl Cyclases↗

PubMed1995

Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland.

The purpose of this study was to investigate the mechanisms involved in the reduced thyroid function in starved, young female rats. Food deprivation for 3 days reduced the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA, the amount of proTRH-derived peptides (TRH and proTRH160-169) in the paraventricular nucleus, the release of proTRH-derived peptides into hypophysial portal blood and the pituitary levels of TSH beta mRNA. Plasma TSH was either not affected or slightly reduced by starvation, but food deprivation induced marked increases in plasma corticosterone and decreases in plasma thyroid hormones. Refeeding after starvation normalized these parameters. Since the molar ratio of TRH and proTRH160-169 in hypophysial portal blood was not affected by food deprivation, it seems unlikely that proTRH processing is altered by starvation. The median eminence content of pGlu-His-Pro-Gly (TRH-Gly, a presumed immediate precursor of TRH), proTRH160-169 or TRH were not affected by food deprivation. Since median eminence TRH-Gly levels were very low compared with other proTRH-derived peptides it is unlikely that alpha-amidation is a rate-limiting step in hypothalamic TRH synthesis. Possible negative effects of the increased corticosterone levels during starvation on proTRH and TSH synthesis were studied in adrenalectomized rats which were treated with corticosterone in their drinking water (0.2 mg/ml). In this way, the starvation-induced increase in plasma corticosterone could be prevented. Although plasma levels of thyroid hormones remained reduced, food deprivation no longer had negative effects on hypothalamic proTRH mRNA, pituitary TSH beta mRNA and plasma TSH in starved adrenalectomized rats. Thus, high levels of corticosteroids seem to exert negative effects on the synthesis and release of proTRH and TSH. This conclusion is corroborated by the observation that TRH release into hypophysial portal blood became reduced after administration of the synthetic glucocorticosteroid dexamethasone. On the basis of these results, it is suggested that the reduced thyroid function during starvation is due to a reduced synthesis and release of TRH and TSH. Furthermore, the reduced TRH and TSH synthesis during food deprivation are probably caused by the starvation-induced enhanced adrenal secretion of corticosterone.

Adrenal Glands↗

PubMed1994

Pharmacological characterization of somatostatin receptors in rat cerebellar nuclei.

Rat cerebellar nuclei contain somatotropin release-inhibiting factor (SRIF) receptors that bind [125I][Leu8,D-Trp22,Tyr25]SRIF-28 but do not bind [125I][Tyr0,D-Trp8]SRIF-14. The aim of the present study was to investigate the pharmacological profile of these receptors by means of binding experiments on tissue sections and quantitative autoradiography. Competition experiments indicated the presence of a single class of [125I][Leu8,D-Trp22,Tyr25]SRIF-28 binding sites in the lateral cerebellar nuclei, showing similar affinities for SRIF-14 and SRIF-28, but low affinity for short-chained analogs. The IC50 values for somatostatin analogs to compete with the binding of [125I][Leu8,D-Trp22,Tyr25]SRIF-28 in the lateral cerebellar nuclei ranked as follows: [Leu8,D-Trp22,Tyr25]SRIF-28 approximately SRIF-14 approximately SRIF-28 < CGP 23996 < D-Phe-Phe-Phe-D-Trp-Lys-Thr-Phe-Thr-NH2 (BIM 23052) < SMS 201-995 approximately N-Ahep-(7-10)SRIF-14-Bzl << MK 678 < D-Phe-Phe-Tyr-D-Trp-Lys-Val-Phe-D-Nal-NH2 (BIM 23056) < D-Phe-c[Cys-Tyr-D-Trp-Lys-Abu-Cys]Nal-NH2 (NC 8-12). Optimum binding of [125I][Leu8,D-Trp22,Tyr25]SRIF-28 did not require divalent cations, and was partly inhibited by guanosine 5' triphosphate. It appears from this study that the rat lateral cerebellar nuclei contain a pure population of receptors exhibiting the same binding characteristics as the recently cloned sstr1 somatostatin receptor. These nuclei could thus provide a useful model in which to investigate the characteristics of native sstr1.

Amino Acid Sequence↗

PubMed1994

Inhibitory effect of adenosine on electrical activity of frog melanotrophs mediated through A1 purinergic receptors.

1. The effects of adenosine were studied in cultured frog melanotrophs by the patch-clamp technique. 2. In cell-attached experiments, most cells responded to adenosine (50 microM) by a reversible inhibition of action current discharges without any apparent desensitization. 3. In whole-cell experiments, adenosine provoked a hyperpolarization accompanied by a depression of spontaneous action potentials and a decrease in membrane resistance. When adenosine was repeatedly applied, tachyphylaxis was observed. Addition of GTP (100 microM) in the intracellular solution augmented the percentage of cells hyperpolarized by adenosine, and the duration and amplitude of the hyperpolarization, and prevented the tachyphylaxis. 4. Pretreatment with pertussis toxin (1 microgram ml-1) blocked adenosine-induced inhibition. 5. In cells dialysed with the non-hydrolysable GTP analogue GTP gamma S (100 microM), adenosine caused a sustained, strong hyperpolarization and an irreversible inhibition of spikes. 6. The effect of adenosine was mimicked by the A1 receptor agonist R-PIA (R-N6-phenylisopropyl-adenosine; 50 microM) and blocked by the A1 receptor antagonist CPDPX (8-cyclopentyl-1,3-dipropylxanthine, 50 microM). The A2 receptor antagonist CGS15943 (9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolo[1,5-c] quinazoline-5-imine; 50 microM) did not affect the adenosine-induced response. 7. The results suggest that, in frog melanotrophs, adenosine exerts a direct hyperpolarizing effect accompanied by blockage of spontaneous action potentials. The effect of adenosine is mediated through A1 receptors coupled to a Gi/o protein.

Action Potentials↗

PubMed1994

Functional characterization of a nonclassical nicotine receptor associated with inositolphospholipid breakdown and mobilization of intracellular calcium pools.

Classical nicotinic receptors are neurotransmitter-gated channels that, upon activation by acetylcholine, induce the opening of an intrinsic cationic channel. We have recently observed that, in frog pituitary melanotrophs, nicotine stimulates alpha-melanocyte-stimulating hormone (alpha-MSH) release through a noncholinergic mechanism. In the study reported here, we investigated the intracellular events that mediate the response of frog melanotrophs to nicotine. Nicotine was capable of stimulating alpha-MSH release in the absence of Ca2+ and/or Na+ in the extracellular medium. A short pulse of nicotine induced a rapid and transient increase of cytosolic free Ca2+ concentration ([Ca2+]i). The effect of nicotine on Ca2+ mobilization was not affected in the absence of Na+ and Ca2+ in the extracellular medium, indicating that the nicotine-evoked increase in [Ca2+]i did not result from Na+ or Ca2+ influx. Nicotine induced both an increase in inositol trisphosphate and a reduction in phosphaditylinositol bisphosphate concentrations but did not affect cAMP production. The present results indicate that nicotine-induced stimulation of alpha-MSH release in frog melanotrophs can be explained by activation of inositolphospholipid breakdown and mobilization of inositol triphosphate-dependent intracellular Ca2+ pools. These data provide evidence for the existence of an unusual type of noncholinergic nicotine receptor positively coupled to phospholipase C.

Animals↗

PubMed1994

Effect of a series of 5-HT4 receptor agonists and antagonists on steroid secretion by the adrenal gland in vitro.

We have previously shown that serotonin (5-hydroxytryptamine, 5-HT) stimulate corticosterone and aldosterone secretion from perifused frog adrenal gland in vitro through activation of 5-HT4 receptors. In the present study, we have used this model to investigate the effect of newly discovered 5-HT4 receptor agonists and antagonists on corticosteroid secretion. Serotonin, the benzamide derivatives (R,S)-zacopride ((R,S)-4-amino-N-(1- azabicyclo[2.2.2]oct-3-yl)-5-chloro-2-methoxybenzamide, HCI) and its enantiomers, the azabicycloalkyl benzimidazole derivatives BIMU 1 (endo-N- (8-methyl-8-azabicyclo-[3.2.1]oct-3-yl)-2,3-dihydro-3-ethyl-2-oxo- 1H-benzimidazole-1-carboxamide, HCl) and BIMU 8 (endo-N-(8-methyl-8- azabicyclo-[3.2.1]oct-3-yl)-2,3-dihydro-(1-methyl)ethyl-2-oxo-1H- benzimidazole-1-carboxamide, HCl) were all capable of enhancing corticosterone and aldosterone secretion in a dose-dependent manner. Serotonin was the most potent stimulator of steroidogenesis (EC50 = 1.5 x 10(-7) M) while the potency of the benzamide and the benzimidazolone derivatives was approximately 10 times lower. The rank order of efficacy of the different 5-HT4 receptor agonists was: (S)-zacopride > BIMU 8 = (R,S)-zacopride > BIMU 1 = (R)-zacopride = 5-HT. The stimulatory effects of 5-HT and the benzimidazolone derivatives on corticosteroid secretion were not additive, suggesting that they activated the same receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1994

Skin peptide tyrosine-tyrosine, a member of the pancreatic polypeptide family: isolation, structure, synthesis, and endocrine activity.

Pancreatic polypeptide, peptide tyrosine-tyrosine (PYY), and neuropeptide tyrosine (NPY), three members of a family of structurally related peptides, are mainly expressed in the endocrine pancreas, in endocrine cells of the gut, and in the brain, respectively. In the present study, we have isolated a peptide of the pancreatic polypeptide family from the skin of the South American arboreal frog Phyllomedusa bicolor. The primary structure of the peptide was established as Tyr-Pro-Pro-Lys-Pro-Glu-Ser-Pro-Gly-Glu10-Asp-Ala-Ser-Pro-Glu-Glu- Met-Asn- Lys-Tyr20-Leu-Thr-Ala-Leu-Arg-His-Tyr-Ile-Asn-Leu30-Val-Thr- Arg-Gln-Arg-Tyr-NH2 . This unusual peptide, named skin peptide tyrosine-tyrosine (SPYY), exhibits 94% similarity with PYY from the frog Rana ridibunda. A synthetic replicate of SPYY inhibits melanotropin release from perifused frog neurointermediate lobes in very much the same way as NPY. These results demonstrate the occurrence of a PYY-like peptide in frog skin. Our data also suggest the existence of a pituitary-skin regulatory loop in amphibians.

Amino Acid Sequence↗

PubMed1994

Ontogeny of pituitary adenylate cyclase-activating polypeptide (PACAP) receptors in the rat cerebellum: a quantitative autoradiographic study.

Pituitary adenylate cyclase-activating polypeptide and PACAP receptors are both present in the rat cerebellar cortex, suggesting that PACAP may play an important role in the cerebellum. In the present study, the variation of the concentration of PACAP binding sites in the rat cerebellum was investigated during postnatal development by means of quantitative autoradiography, using [125I]PACAP27 as a radioligand. In the external granule cell layer and the medulla, the density of PACAP binding sites was high at birth, markedly decreased from postnatal day 8 (P8) to P25 and finally vanished at the end of the third postnatal week. In the internal granule cell layer and molecular layer, PACAP binding sites were first detected at P8. In the internal granule cell layer, the density of binding sites slightly decreased during development but remained elevated in adults. Conversely, in the molecular layer, PACAP binding sites rapidly decreased during the second and third postnatal weeks and virtually disappeared after P25. In all four layers of the cerebellar cortex, the autoradiographic labeling was displaced by PACAP27 (IC50 close to 10(-8) M), but was not affected by VIP. No significant changes in IC50 and Hill coefficient were noticed in the various layers throughout development. The present study shows that all four layers of the cerebellar cortex express PACAP binding sites during development. The evolution of the receptor concentration exhibited differential profiles in the various layers but the specificity characteristics of the recognition sites were identical in all four structures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1994

Immunocytochemical evidence for the presence of Met-enkephalin and Leu-enkephalin in distinct neurons in the brain of the elasmobranch fish Scyliorhinus canicula.

Immunohistochemical methods have been used to investigate the distribution of various opioid peptides derived from mammalian proenkephalin in the central nervous system of Scyliorhinus canicula. The results indicate that both Leu- and Met-enkephalin-immunoreactive peptides are present in the dogfish brain. In contrast, enkephalin forms similar to Met-enkephalin-Arg-Phe or Met-enkephalin-Arg-Gly-Leu, and mammalian alpha-neo-endorphin, dynorphin A (1-8), dynorphin A (1-13), and dynorphin A (1-17) were not detected. Met- and Leu-enkephalin immunoreactivities were found in distinct neurons of the telencephalon and hypothalamus. In particular, cell bodies reacting only with the Met-enkephalin antiserum were localized in the preoptic nucleus and in the suprachiasmatic region of the hypothalamus. Conversely, cell bodies reacting only with the Leu-enkephalin antiserum were localized in the pallium and the nucleus lobi lateralis hypothalami. Several areas of the telencephalon and diencephalon exhibited both Met- and Leu-enkephalin-like immunoreactivity, but the two immunoreactive peptides were clearly contained in distinct perikarya. The overall distribution of Met-enkephalin-immunoreactive elements in the dogfish exhibited similarities to the distribution of proenkephalin-derived peptides previously reported for the brain of tetrapods. The fact that Met- and Leu-enkephalin-like peptides were detected in distinct neurons, together with the absence of dynorphin-related peptides, suggests the existence of a novel Leu-enkephalin-containing precursor in the dogfish brain.

Amino Acid Sequence↗

PubMed1994

Intracerebroventricular administration of angiotensin II increases heart rate in the conscious trout.

The central effect of angiotensin II on cardiovascular activity has been investigated in conscious trout bearing an intracerebroventricular (i.c.v.) cannula and an intra-arterial catheter. I.c.v. injection of the angiotensin II agonist [Asn1,Val5]AII (6.2-50 pmol) induced a dose-dependent increase in heart rate and arterial blood pressure. Central administration of the angiotensin II antagonist DuP 753 (5 nmol) 30 min before i.c.v. injection of [Asn1,Val5]AII totally prevented the tachycardia and reduced the hypertension induced by the angiotensin II agonist. Intra-arterial injection of arginine-vasotocin (12.5 pmol) caused a bradycardia associated with a marked increase in arterial blood pressure. I.c.v. injection of [Asn1,Val5]AII totally blocked the bradycardia induced by arginine-vasotocin and this effect was prevented by central administration of DuP 753. In contrast, [Asn1,Val5]AII did not affect the increase in blood pressure induced by arginine vasotocin. Suppression of the vagal tone by atropine treatment totally blocked the central effect of [Asn1,Val5]AII. These results show that angiotensin II acts directly on the trout brain to increase blood pressure and heart rate. The effect of angiotensin II is mediated through a receptor related to the mammalian AT1 receptor type.

Angiotensin II↗

PubMed1994

Frog diazepam-binding inhibitor: peptide sequence, cDNA cloning, and expression in the brain.

Three peptides derived from diazepam-binding inhibitor (DBI) were isolated in pure form from the brain of the frog Rana ridibunda. The primary structures of these peptides showed that they correspond to mammalian DBI-(1-39), DBI-(58-87), and DBI-(70-87). A set of degenerate primers, whose design was based on the amino acid sequence data, was used to screen a frog brain cDNA library. The cloned cDNA encodes an 87-amino acid polypeptide, which exhibits 68% similarity with porcine and bovine DBI. Frog DBI contains two paired basic amino acids (Lys-Lys) at positions 14-15 and 62-63 and a single cysteine within the biologically active region of the molecule. Northern blot analysis showed that DBI mRNA is expressed at a high level in the brain but is virtually absent in peripheral tissues. The distribution of DBI mRNA and DBI-like immunoreactivity in the frog brain was studied by in situ hybridization and immunocytochemistry. Both approaches revealed that the DBI gene is expressed in ependymal cells and circumventricular organs lining the ventricular cavity. Since amphibia diverged from mammals at least 250 million years ago, the data show that evolutionary pressure has acted to conserve the structure of DBI in the vertebrate phylum. The distribution of both DBI mRNA and DBI-like immunoreactivity indicates that DBI is selectively expressed in glial cells.

Amino Acid Sequence↗

PubMed1994

Melanostatin (NPY) inhibited electrical activity in frog melanotrophs through modulation of K+, Na+ and Ca2+ currents.

1. Melanostatin, a thirty-six amino acid peptide recently isolated from the frog brain due to its ability to inhibit alpha-melanocyte-stimulating hormone (alpha-MSH) release, is the amphibian counterpart of mammalian neuropeptide Y (NPY). The effect of synthetic melanostatin on the bioelectrical activity of cultured frog melanotrophs was studied in 124 cells by using the whole-cell patch-clamp technique. 2. In current-clamp experiments, melanostatin (1 microM) provoked a reversible hyperpolarization and a suppression of spontaneous action potentials. In some cells the hyperpolarizing response was absent, but an arrest of spike firing still occurred. 3. Melanostatin-induced hyperpolarization was associated with a decrease in membrane resistance. In voltage-clamp experiments, melanostatin induced an outward current at a constant command potential. This hyperpolarizing outward current appeared to be carried by potassium ions. 4. Cell dialysis with the non-hydrolysable GTP analogue guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) sustained the outward current produced by melanostatin. Dopamine (1 microM), which generates a similar hyperpolarizing outward current in frog melanotrophs, was not capable of increasing the current provoked by melanostatin and sustained by GTP gamma S. 5. Melanostatin also modulated voltage-operated currents. The amplitude of voltage-activated potassium current was increased by 30%. 6. Melanostatin reduced the fast sodium current. This inhibitory effect was rather persistent compared to the other modulated currents. 7. Melanostatin markedly scaled down high voltage-activated N- and L-like calcium currents. The activation kinetics of these two calcium currents were not altered by the peptide. 8. Pretreatment of melanotrophs with pertussis toxin (1 microgram ml-1) blocked melanostatin-induced inhibition of N- and L-like calcium currents. 9. It is concluded that the NPY-related peptide melanostatin generates a very complex pattern of electrical responses in frog melanotrophs, including hyperpolarization and modulation of voltage-activated currents underlying action potentials. G proteins appear to mediate at least part of these effects.

Action Potentials↗

PubMed1994

In vitro study of olfactory receptor neurones expressing the dipeptide carnosine.

Olfactory neuroepithelial (OE) cells were dissociated from late stage embryonic mice and analysed for carnosine expression. The yield of carnosine neurones was twice as high when the OE cells were seeded along with the olfactory bulb cells. Carnosine neurones resulted from both in vitro survival and neurogenesis, and were associated with clusters of underlying flat cells immunopositive for keratin. Our results demonstrate that olfactory neurones expressing their neurotransmitter carnosine can be studied in culture, and the close association with keratin-immunopositive basal cells suggests that they are dependent on these cells for survival and/or differentiation.

Animals↗

PubMed1994

Effect of chronic treatment with the antidepressant tianeptine on the hypothalamo-pituitary-adrenal axis.

The effects of acute and chronic administration of tianeptine, a novel antidepressant agent, on the hypothalamo-pituitary-adrenal axis were studied in the adult male rat. A single injection of tianeptine did not alter the activity of the hypothalamo-pituitary-adrenal axis. In contrast, chronic administration of tianeptine (10 mg/kg twice a day for 15 days) induced a significant decrease in the concentration of corticotropin-releasing factor (CRF) in the hypothalamus and adrenocorticotropin (ACTH) in the anterior lobe of the pituitary. Chronic tianeptine treatment did not modify CRF levels in the cerebral cortex and hippocampus, and did not alter alpha-melanocyte-stimulating hormone and beta-endorphin levels in the neurointermediate lobe of the pituitary. Using the in situ hybridization technique, we observed that chronic administration of tianeptine did not modify CRF mRNA levels in the paraventricular nucleus of the hypothalamus. The effect of chronic tianeptine treatment on the neuroendocrine response to stress was also investigated. Tube restraint stress for 30 min induced a significant depletion of hypothalamic CRF and a substantial increase of plasma ACTH and corticosterone. Tianeptine abolished the stress-induced reduction of hypothalamic CRF concentration and markedly reduced the stress-induced increase in plasma ACTH and corticosterone levels. Taken together, these results suggest that tianeptine acts primarily at the level of the hypothalamus: (1) in unstressed rats, tianeptine reduces hypothalamic CRF and pituitary ACTH contents; (2) in stressed animals, tianeptine attenuates the activation of the hypothalamo-pituitary-adrenal axis.

Animals↗

PubMed1994

Effect of basic fibroblast growth factor and alpha-melanocytic stimulating hormone on nerve regeneration through a collagen channel.

An experimental study on the rat sciatic nerve was performed to evaluate nerve regeneration through a collagen guide and to study the effects of alpha-melanocytic stimulating hormone (alpha-MSH) and basic fibroblast growth factor (b-FGF) in accelerating axonal elongation. After transection, nerves were repaired over a 7 mm gap using a placental collagen type IV guide. The channel was filled with either a b-FGF solution or an alpha-MSH solution or was produced with b-FGF incorporated into the guide. Four weeks later, only groups in which b-FGF had been injected or incorporated displayed a significant somatosensory evoked potential response. Histological and quantitative analysis of nerve fibres confirmed the existence of nerve continuity in groups receiving an alpha-MSH solution or a channel containing b-FGF. These results demonstrate that alpha-MSH in solution and b-FGF incorporated into a collagen type IV channel enhance peripheral nerve regeneration. However, at 4 weeks, only b-FGF (3 ng) restores functional activity.

Animals↗

PubMed1994

Spasmogenic actions of frog urotensin II on the bladder and ileum of the frog, Rana catesbeiana.

The effects of synthetic frog urotensin II on the motility of isolated smooth muscle strips of urinary bladder and ileum from the bullfrog Rana catesbeiana were investigated. The strips of bladder exhibited strong spontaneous contractions. Frog urotensin II produced a concentration-dependent increase in the frequency of contraction (EC50 = 8.1 x 10(-9) M) but had no significant effect on tension. Maximum stimulation (4 times the rate of spontaneous contractions) was produced by 10(-7) M peptide. The ileal smooth muscle strips exhibited only weak spontaneous contractions but frog urotensin II produced concentration-dependent increases in both the frequency (EC50 = 1.3 x 10(-9) M) and the strength (EC50 = 3.6 x 10(-9) M) of contraction. The peptide had no effect on the motility of strips of rat urinary bladder and ileum. In both the frog bladder and ileum preparations, the effect of urotensin II was not affected by preincubation of the strips with atropine, tetrodotoxin, and somatostatin-14 but indomethacin produced a significant (P < 0.05) decrease in the strength of the contractions of the bladder (to 21 +/- 6% of control values) and ileum (to 32 +/- 13%). Arachidonic acid produced an increase in the frequency of contraction of the bladder and an increase in both the frequency and the strength of contraction of the ileum. The data demonstrate that urotensin II exercises a spasmogenic effect on amphibian smooth muscle that is similar to that of the peptide on teleost tissues. An involvement of prostaglandin synthesis in the spasmogenic action of urotensin II on frog bladder and ileum is indicated.

Animals↗

PubMed1994

Localization of diazepam-binding inhibitor and peripheral type benzodiazepine binding sites in the rat ovary.

Diazepam-binding inhibitor (DBI) is the precursor of a family of peptides, including an octadecaneuropeptide (ODN), that share with DBI the ability to specifically displace benzodiazepines (BZD) from their receptors. An association of ODN with the peripheral type BZD receptors (PBR) has been reported in the brain and a few peripheral tissues. In order to investigate whether DBI and PBR are present in ovarian tissue, we have localized DBI by means of immunocytochemistry, in situ hybridization and autoradiography of PBR in the rat ovary. Immunocytochemical localization was achieved by means of rabbit antibodies developed against rat ODN. Immunostaining was located in the cytoplasm of the theca interna, corpus luteum and interstitial gland cells, but not in the granulosa cells. Hybridization signal obtained following in situ hybridization with a [35S]-labelled single-stranded RNA probe complementary to DBI mRNA was observed in all the steroid-secreting cells, including granulosa cells of developing and mature follicles. Autoradiographic localization of PBR obtained by incubating ovary sections with [3H] PK11195, a ligand selective for PBR, revealed the presence of specific labelling in all the steroid-secreting cells. These results, which demonstrate for the first time that the ovarian steroid-secreting cells contain both PBR and its endogenous ligand, suggest that the BZD receptor might be involved in the regulation of ovarian function.

Animals↗