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H Vaudry

Publications and source records attributed to H Vaudry.

At least 415 records · Page 23Linked to original sources
PubMed1990

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe.

Previous studies have demonstrated that TRH is a potent stimulator of alpha-MSH secretion from frog pituitary melanotrophs. In order to determine the intracellular events responsible for TRH-evoked alpha-MSH release, we have investigated the effect of TRH on polyphosphoinositide breakdown in frog pars intermedia. Neurointermediate lobes were labelled to isotopic equilibrium with myo-[3H]inositol. TRH stimulated the rate of incorporation of [3H]inositol into the phospholipid fraction. The effect of TRH was concentration-dependent; half-maximal stimulation of alpha-MSH release and inositol incorporation occurred at 12 and 28 nmol TRH/l respectively. In prelabelled neurointermediate lobes, lithium (10 mmol/l) enhanced the radioactivity in inositol monophosphate, bisphosphate (IP2) and trisphosphate (IP3). LiCl (10 mmol/l) induced a 38% inhibition of alpha-MSH release from perifused neurointermediate lobes but did not impair TRH-induced alpha-MSH secretion. In the presence of LiCl, TRH (1 mumol/l) induced a transient increase of the radioactivity in IP3, which was evident by 30 s and maximal by 1 min (+100%). TRH treatment also increased the radioactivity in IP2, which reached a plateau after 5 min (+100%). The increase in radioactivity in IP3 induced by TRH was closely paralleled by a rapid loss of [3H]phosphatidylinositol bisphosphate (PIP2), which was maximal by 1 min (-70%). These results indicate that, in frog pars intermedia, TRH-evoked alpha-MSH secretion is coupled to breakdown of PIP2. The data suggest that, in amphibian melanotrophs, as previously shown in GH3 tumour cells and in rat pituitary mammotrophs, TRH causes rapid stimulation of polyphosphoinositide-hydrolysing phospholipase C.

Animals↗
PubMed1990

[A cellular anti-ischemic agent, trimetazidine prevents the deleterious effects of oxygen free-radicals on the internal ear].

Improvement of cochleovestibular symptoms induced by trimetazidine (TMZ) has been evidenced by clinical studies. However, a poor knowledge of the physiopathology and the scarcity of experimental models contributed to making determination of the mode of action of the drugs difficult. We studied the effect, in vitro, of TMZ on the production of oxygen-derived free radicals using, as a biological model, the isolated semicircular canal of the frog. This model allows to exert separate control over the ionic composition of the endo- and perilymphatic fluids. The spontaneous activity of the afferent nerve fibers, as well as the endolymphatic potential, were recorded at rest. Three additional parameters were analyzed, while the semicircular canal was subjected to mechanical stimulation, i.e., ampulla potential, nerve potential and the evoked frequency of action potentials. Free radical generation induced by the administration of phenazine methosulfate (PMS, 10(-5) M, 15 min) into the perilymphatic compartment, leads to a deterioration of the production of endolymph and the release of this afferent neuromediator. Inversely, PMS has no influence whatsoever on the mechanisms of mechanical-electrical transduction. The addition of TMZ (10(-6) or 10(-5) M) in the perilymphatic compartment counteracts the harmful effects of free radicals on the various bioelectric activities. These results suggest that the beneficial action of TMZ observed during treatment of cochleovestibular disorders is due, at least in part, to the anti-oxidizing properties of the molecule of interest.

Action Potentials↗
PubMed1989

Effect of phenazine methosulfate on electrophysiological activity of the semicircular canal: antioxidant properties of trimetazidine.

Ischemia strokes appear to be the main source of cochleo-vestibular dysfunctions of peripheral origin. The present study aimed to investigate the action of oxygen free radicals on the bioelectric activity of the labyrinthine epithelium, using the frog semicircular canal as an in vitro preparation. We also examined the possible effect of the antianginal drug, trimetazidine (TMZ), under physiological conditions and during the administration of phenazine methosulfate (PMS). The model allows the ionic composition of endolymphatic and perilymphatic fluids bathing the semicircular canal to be dealt with separately. Spontaneous afferent vestibular nerve activity and the endolymphatic potential were recorded under resting conditions. Three additional parameters were investigated during mechanical displacement of the endolymphatic fluid: the ampullar direct current, the nerve direct current and the frequency of the evoked afferent spikes. Addition of TMZ (10(-6) and 10(-5) M, 50 min) into the perilymphatic compartment did not induce significant modifications of the different bioelectrical signals. Generation of oxygen free radicals, through administration of PMS (10(-5) M, 15 min) into the perilymphatic compartment, caused an impairment of all bioelectrical signals, except the ampullar direct current. The spontaneous activity, nerve direct current and frequency of afferent evoked spikes signals were significantly reduced 75 min after the start of PMS administration (-64, -17 and -32%, respectively). In contrast, there was a marked increase of the endolymphatic potential signal (+51%). Addition of TMZ (10(-6) or 10(-5) M) into the perilymph solution reversed the effect of PMS on all bioelectrical signals. These results indicate that TMZ acts as an antioxidant molecule which is capable of protecting the labyrinthine epithelium from the deleterious effect of oxygen radicals. Our data suggest that the protective effect of TMZ on ischemia-induced cochleo-vestibular dysfunctions may be accounted for by the antioxidant properties of this antianginal drug.

Animals↗
PubMed1989

gamma-Aminobutyric acid inhibits the release of alpha-melanocyte-stimulating hormone from rat hypothalamic slices.

The effect of gamma-aminobutyric acid (GABA) on release of alpha-melanocyte-stimulating hormone (alpha-MSH) from hypothalamic neurons was investigated in vitro using the perifusion technique. Rat hypothalamic slices were continuously superfused with Krebs-Ringer medium and the release of alpha-MSH in the effluent perifusate was monitored by means of a sensitive and specific radioimmunoassay method. Infusion of 50 mM K+ for 15 min induced a transient increase of alpha-MSH release (5- to 8-fold above the spontaneous level). Infusion of the same dose of K+ for 75 min caused a brief discharge of alpha-MSH during the first 30 min followed by sustained release of the neuropeptide. The effect of GABA was investigated 27 min after the onset of KCl infusion. Application of GABA (5 x 10(-5) M) resulted in a significant and reversible inhibition of K+-induced alpha-MSH release. The GABAA agonist, muscimol (10(-4) M), produced a prolonged inhibition of K+-evoked alpha-MSH release, while the GABAB agonist, baclofen (10(-4) M), was devoid of effect on hypothalamic alpha-MSH release. Bicuculline (10(-4) M), a specific GABAA antagonist, had no effect when added alone to the medium but totally reversed the inhibitory effect of GABA on K+-induced alpha-MSH release. Taken together, these data suggest that exogenous GABA exerts an inhibitory control on alpha-MSH neurons. Our data also show that the effect of GABA on alpha-MSH release by hypothalamic neurons is mediated through GABAA-type receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminooxyacetic Acid↗
PubMed1989

Localization of atrial natriuretic factor (ANF) binding sites in the central nervous system of the frog.

The distribution of atrial natriuretic factor (ANF) binding sites was investigated in the central nervous system of the frog Rana ridibunda using the technique of in vitro receptor autoradiography by means of [125I]-labeled ANF-28. The anatomic distribution of ANF recognition sites was determined on Kodak ARX films apposed onto tissue sections, and their distribution was examined in greater detail by analysis of autoradiograms generated by using emulsion-coated sections. The highest levels of ANF binding sites were found in the olfactory bulb, the dorsal pallium, the septum, the habenular nucleus, the dorsal infundibular nucleus, the interpeduncular nucleus, and in the tectum. Moderate levels of ANF binding sites were observed in the thalamus and throughout the mesencephalon, whereas low levels were detected in the lateral and medial pallium, the medial forebrain bundle, and the nucleus rotondus. In the pituitary gland, the neural and distal lobes were densely loaded with ANF binding sites, whereas no autoradiographic labeling was observed in the pars intermedia. In general, there was a good correlation between the location of ANF receptors and the distribution of ANF-containing neurons, as previously determined by immunocytochemistry. Together these results support the view that ANF may act as a neurotransmitter or a neuromodulator in various regions of the frog brain.

Animals↗
PubMed1989

Distribution of somatostatin receptors in the brain of the frog Rana ridibunda: correlation with the localization of somatostatin-containing neurons.

The biochemical characterization and anatomical distribution of somatostatin binding sites were examined in the brain of the frog Rana ridibunda, and the distribution of the receptors was compared with the location of somatostatin immunoreactive neurons. The pharmacological profile of somatostatin receptors was determined in the frog brain by means of an iodinated superagonist of somatostatin, [125I-Tyr0,DTrp8]S-14. Membrane-enriched preparations from frog brain homogenates were shown to contain high-affinity receptors (KD = 0.78 +/- 0.34 nM; Bmax = 103 + 12.7 fmoles/mg protein) with pharmacological specificity for [DTrp] substituted S14 and S28 analogs. The distribution of somatostatin-binding sites was studied by autoradiography on coronal sections of frog brain. Various densities of somatostatin receptors were detected in discrete areas of the brain. The highest concentration of binding sites was observed in the olfactory bulb, in the pallium, and in the superficial tectum. Moderate binding was observed in the striatum, amygdaloid complex, preoptic area, and cerebellum. Immunocytochemical studies of the distribution of somatostatin-28 (S28) related peptides were also conducted in the frog brain. Two antisera that recognize distinct epitopes of the somatostatin molecule have been used for immunohistochemical mapping of the peptide. Antiserum SS9 recognizes both S28 and somatostatin-14 (S14) and allowed the labelling of perikarya. Antiserum S320 recognizes the N-terminal fragment (1-12) resulting from enzymatic cleavage of S28. This latter antiserum, which does not cross-react with S28, stained mainly neuronal processes. At the infundibular level, however, both antisera stained cell bodies and fibers. Immunoreactive somatostatin-related peptides were detected in many areas of the frog brain. In the diencephalon, a heavy accumulation of perikarya and fibers was seen in the preoptic nucleus, the dorsal and ventral infundibular nuclei, and the median eminence. Immunoreactive perikarya were also observed in the telencephalon, especially in the pallium and in thalamic nuclei. Immunostained processes were detected in many telencephalic areas and in the tectum. There was good correlation between the distribution of somatostatin-immunoreactive elements and the location of somatostatin-binding sites in several areas of the brain, in particular in the median pallium, the tectum, and the interpeduncular nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Localization and characterization of prolactin-like immunoreactivity in the pituitary of the frog Rana ridibunda.

Distribution and quantification of PRL in the pituitary gland of the frog Rana ridibunda were investigated using a high-affinity antiserum raised against bullfrog prolactin (PRL). The immunoreactive PRL-producing cells were distributed throughout the pars distalis, the highest density of cells being observed in the rostral region of the adenohypophysis facing the neurointermediate lobe. The dorsal region of the pars distalis contained only a few scattered PRL-immunoreactive cells. At the electron microscopic level, PRL-containing cells were visualized using the immunogold procedure. PRL-immunoreactive material was exclusively stored in secretory granules (size ranging from 200 to 700 nm in diameter). Neither the rough endoplasmic reticulum nor the Golgi apparatus were immunolabeled. Using a radioimmunoassay method we have compared the displacement curves obtained with bullfrog PRL and acetic extracts from Rana ridibunda pituitary. The two binding curves were not completely parallel, suggesting the existence of slight variations of the amino acid sequences of PRL in the two species. The concentration of PRL in the green frog adenohypophysis appeared somewhat higher (35.3 +/- 8.8 micrograms/mg protein) than that in the bullfrog pituitary. These results validate the use of an antiserum to bullfrog PRL to investigate the regulation of PRL secretion in Rana ridibunda.

Animals↗
PubMed1989

Mechanism of action of serotonin on frog adrenal cortex.

The mechanism of action of serotonin (5-HT) on frog adrenal cortex has been investigated in vitro using the perifusion system technique. The direct effect of 5-HT on corticosteroid secreting cells was demonstrated, using enzymatically dispersed adrenocortical cells. Melatonin and 5-HTP appeared to be less potent than 5-HT to enhance corticosteroid secretion. In contrast Trp and 5-HIAA were totally devoid of effect on steroid secretion. To investigate the type of receptor involved in the stimulatory effect of 5-HT on adrenocortical cells, adrenal slices were stimulated with 5-HT in absence or presence of various antagonists. We observed that classical antagonists of 5-HT1, 5-HT2 and 5-HT3 type receptors failed to block 5-HT-induced corticosteroid secretion in our model. These results show that 5-HT exerts a direct effect on corticosteroid-secreting cells. Our data also indicates that the type of receptor involved in the action of 5-HT in frog adrenal cortex differs from mammalian 5-HT receptors.

5-Hydroxytryptophan↗
PubMed1989

Dopamine inhibits corticosteroid secretion in frog adrenocortical cells: evidence for the involvement of prostaglandins in the mechanism of action of dopamine.

We have investigated the possible involvement of arachidonic acid metabolites in dopamine-induced inhibition of adrenocortical steroidogenesis. Administration of dopamine (5 x 10(-5) M) for 20 min to perifused frog adrenal slices caused a marked reduction of the release of both prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha, the stable metabolite of prostacyclin (PGI2). Dopamine also induced a significant inhibition of corticosterone and aldosterone secretion. A lag period of 20 min was observed between inhibition of prostanoid and corticosteroid releases. Prolonged dopamine infusion did not prevent the stimulatory effect of PGE1, PGE2 or arachidonic acid on corticosteroid secretion. These observations indicate that activation of dopaminergic receptors in adrenocortical cells is linked to an inhibition of arachidonic acid metabolism. Our data also suggest that the inhibitory effect of dopamine occurs at a step preceding arachidonic acid formation.

Adrenal Cortex↗
PubMed1989

Melanin concentrating hormone. V. Isolation and characterization of alpha-melanocyte-stimulating hormone from frog pituitary glands.

The structure of alpha-melanocyte-stimulating hormone (alpha-MSH) has been determined in the pars intermedia of the frog Rana ridibunda. Pulse-chase labeling of frog neurointermediate lobes with selective amino acids revealed that the composition of frog alpha-MSH is similar to that of alpha-MSH from all mammalian species yet studied. Tryptic mapping of nexly synthetized alpha-MSH generated two fragments with the following amino acid composition: (T1) Trp, Pro, Lys, Gly, Val and (T2) Tyr, Arg, Phe, His, Ser, Glu. Concurrently, alpha-MSH was purified from 100 neurointermediate lobes to apparent homogeneity by reverse-phase HPLC. The sequence of the peptide determined by automated Edman degradation was Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val. The structure of frog alpha-MSH is thus identical to mammalian des-N alpha-acetyl alpha-MSH and differs from the sequence of toad (Xenopus laevis) alpha-MSH only by the first residue (Ser instead of Ala). These results confirm that the sequence of alpha-MSH has been highly preserved during evolution.

Amino Acid Sequence↗
PubMed1989

Involvement of voltage-operated calcium channels in alpha-melanocyte-stimulating hormone (alpha-MSH) release from perifused rat hypothalamic slices.

The contribution of voltage-operated calcium (VOC) channels in the mechanism of release of alpha-melanocyte-stimulating hormone (alpha-MSH) from hypothalamic neurons was investigated using perifused rat hypothalamic slices. The stimulatory effect of potassium (50 mM) on alpha-MSH release was completely blocked by cadmium (1 mM) a calcium competitor which indifferently blocks T-, L-and N-type VOC channels. To determine the nature of calcium conductances involved in K+-evoked alpha-MSH release, we have investigated the effect of a VOC channel agonist and 3 antagonists on the secretion of the neuropeptide. Administration of synthetic omega-conotoxin fraction GVIA (1 microM), a peptide toxin which blocks both N- and L-type VOC channels, reduced by 33% K+-induced alpha-MSH release. In contrast, the 1,4-dihydropyridine (DHP) antagonist nifedipine, at concentrations up to 100 microM, did not affect the response of hypothalamic alpha-MSH neurons to depolarizing concentrations of KCl. In addition, the secretion of alpha-MSH induced by high K+ concentrations was not reduced by nifedipine (10 microM) in the presence of diltiazem (1 microM), a benzothiazepine derivative which increases the affinity of the DHP antagonist for L-type VOC channels. The DHP agonist BAY K 8644 (0.1-10 microM) did not modify the early phase of the response of alpha-MSH neurons to K+-induced depolarization. In contrast BAY K 8644 (1 or 10 microM) significantly prolonged the duration of K+-induced alpha-MSH release. This sustained release of alpha-MSH induced by BAY K 8644 (10 microM) was totally suppressed by nifedipine (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Characterization of alpha-MSH-related peptides released from rat hypothalamic neurons in vitro.

Reverse-phase high-performance liquid chromatography analysis, coupled with a sensitive radioimmunoassay for alpha-melanocyte-stimulating hormone (alpha-MSH), was used to characterize the alpha-MSH-related peptides stored in the rat hypothalamus or released from perifused hypothalamic slices. Four peaks of alpha-MSH-like immunoreactivity (alpha-MSH-LI) co-eluting with synthetic des-N alpha-acetyl alpha-MSH, alpha-MSH and their respective sulfoxide derivatives were resolved and quantified. In hypothalamic extract, deacetyl alpha-MSH which was the predominant peptide represented 94.4% of total alpha-MSH-LI content, while the relative amount of alpha-MSH was only 5.6%. Analysis of alpha-MSH-related peptides contained in effluent perifusates showed that deacetyl alpha-MSH and its oxidized form were the major peptides released from neurons in basal conditions or under KCl-induced depolarization (50 mM KCl for 75 min). However, the proportion of acetylated peptide was 3-4 times higher in the perifusion medium than in hypothalamic extracts. Our data indicate that acetylation of des-N alpha-acetyl alpha-MSH may occur during the process of exocytosis. Since acetylation of alpha-MSH markedly increases the behavioural potency of the peptide, these results suggest that regulation of the acetyltransferase activity could be a key mechanism to modulate the bioactivity of alpha-MSH-related peptides in the brain.

Animals↗
PubMed1989

Three distinct thyrotropin-releasing hormone-immunoreactive axonal systems project in the median eminence-pituitary complex of the frog Rana ridibunda. Immunocytochemical evidence for co-localization of thyrotropin-releasing hormone and mesotocin in fibers innervating pars intermedia cells.

The localization of thyrotropin-releasing hormone-immunoreactive structures was investigated in the hypothalamo-hypophyseal complex of the frog, Rana ridibunda, by light and electron microscopy using the conventional indirect immunoperoxidase technique and the immuno-gold technique, respectively. The localization of mesotocin-, vasotocin- and neurophysin-immunoreactive elements was compared to that of thyrotropin-releasing hormone either by comparing homologous fields on serial sections or by staining the same section with two different antibodies. Thyrotropin-releasing hormone-immunoreactive perikarya occurred mainly in the anterobasal periventricular area and dorsal extension of the preoptic nucleus, and in the lateral zone of the infundibular nucleus. In the anterobasal preoptic nucleus, the distribution of thyrotropin-releasing hormone-immunoreactive perikarya partially overlapped that of vasotocin- and mesotocin-containing neurons; however, co-localization of thyrotropin-releasing hormone with either nonapeptide could not be detected there. In contrast, in the caudal extension of the preoptic nucleus, thyrotropin-releasing hormone- and mesotocin-like immunoreactivities were frequently co-localized in the same neurons. In the external zone of the median eminence, abundant networks of thyrotropin-releasing hormone- and vasotocin-immunoreactive nerve fibers were found in the vicinity of portal capillaries, while mesotocin-immunoreactive axons were only found in the internal zone. Using the immuno-gold technique at the electron microscopic level, three distinct thyrotropin-releasing hormone-immunoreactive systems were identified in the median eminence-neurointermediate lobe complex. (1) In the external zone of the median eminence, a conspicuous population of pericapillary endings contained 100-nm dense core vesicles immunoreactive solely for thyrotropin-releasing hormone. (2) In the neural lobe of the pituitary, thyrotropin-releasing hormone immunoreactivity occurred on secretory vesicles in a subpopulation of the mesotocinergic axons containing 160-nm secretory granules; co-localization with vasotocin was never seen. (3) In the intermediate lobe, thyrotropin-releasing hormone- and mesotocin (or neurophysin I)-immunoreactivities were systematically found in the same 120-nm dense core vesicles; these thyrotropin-releasing hormone-/mesotocin-immunoreactive axon terminals frequently made synaptic contacts with melanotropic cells. The possible modulatory effect of mesotocin on thyrotropin-releasing hormone-induced alpha-melanocyte-stimulating hormone secretion was investigated using perifused frog neurointermediate lobes. Administration of graded doses of mesotocin (from 10(-10) to 10(-5) M) did not affect the spontaneous release of alpha-melanocyte-stimulating hormone. In addition, mesotocin (10(-7) and 10(-6) M) did not modify thyrotropin-releasing hormone-evoked alpha-melanocyte-stimulating hormone release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Ontogeny of somatostatin receptors in the rat brain: biochemical and autoradiographic study.

The ontogeny of somatostatin receptors in the rat brain has been studied by both membrane binding assays and in vitro receptor autoradiographic techniques. High levels of somatostatin binding sites were detected in brain of 15-day-old fetuses (E15). The pharmacological characterization of somatostatin binding sites and the regulatory effect of GTP on somatostatin binding at E15 suggest that somatostatin recognition sites correspond to authentic receptors. The values of maximal binding showed important variations throughout pre- and postnatal development. Globally, a marked increase in the total binding capacity was observed between E15 and postnatal day 8 (P8), with a transient fall at birth and P1. After P8, the concentration of somatostatin receptors progressively decreased and the weaning imposed at P21 accentuated the decline of receptor concentration. Although the density of somatostatin binding sites varied considerably, KD values did not change during brain development. Autoradiographic studies showed marked differences in the distribution of somatostatin receptors during ontogenesis. In the cortex, the cortical plate and the subplate zone appeared to contain high densities of binding sites from E15 to P1. However, the cortical layer which exhibited the higher labelling was the intermediate zone, located just beneath the subplate zone. On the contrary, the germinal epithelium bordering the lateral ventricle appeared virtually devoid of somatostatin binding sites. This laminar distribution of binding sites in the cortex disappeared from P4 to P8, in coincidence with the evolution of the underlying histological organization. At these stages, a homogeneous distribution was observed in almost all cortical layers, contrasting with the distribution of somatostatin receptors in the adult, which was restricted to layers IV-VI. In the cerebellar cortex, autoradiographic labelling was first seen at E15. After birth, the density of somatostatin receptors increased dramatically between P4 and P13, while, at P23, the labelling vanished in most lobes of the cerebellum. Taken together, these results show the early appearance of somatostatin receptors in the rat brain. The high density of somatostatin receptors observed in proliferative or pre-migratory areas suggests that somatostatin may be an important factor involved in the organization of the central nervous system.

Aging↗
PubMed1989

Central-type benzodiazepines and the octadecaneuropeptide modulate the effects of GABA on the release of alpha-melanocyte-stimulating hormone from frog neurointermediate lobe in vitro.

The involvement of the GABA-benzodiazepine receptor complex in the regulation of melanotropin secretion has been investigated using perfused frog neurointermediate lobes. The GABAA agonist 3-amino-1 propane sulfonic acid mimicked the biphasic effect of GABA on alpha-melanocyte-stimulating hormone secretion: a brief stimulation followed by an inhibition of melanotropin secretion. The GABAA antagonist SR 95531 (10(-4) M) inhibited both stimulation and inhibition of alpha-melanocyte-stimulating hormone release induced by GABA (10(-4) M). Since the inhibitory effect of baclofen (10(-4) M) was partially antagonized by SR 95531 (10(-4) M), it appears that the GABAergic control of alpha-melanocyte-stimulating hormone release is mainly achieved through activation of GABAA receptors. GABA-induced stimulation of alpha-melanocyte-stimulating hormone release was inhibited by tetrodotoxin (10(-5) M), an Na+ -channel blocker, or nifedipine (10(-5) M), a voltage-dependent Ca2+ -channel blocker, suggesting that Na+ and Ca2+ ions are involved in the stimulatory phase of GABA action. Only central-type benzodiazepine binding site agonists such as clonazepam (10(-4) M) modified alpha-melanocyte-stimulating hormone release. In fact, clonazepam (10(-7) to 10(-5) M) led to a dose-dependent potentiation of both GABA-induced stimulation and inhibition of alpha-melanocyte-stimulating hormone release. This potentiating effect was antagonized by the GABAA antagonist SR 95531 (10(-4) M) or by the central-type benzodiazepine binding site antagonist flumazenil (10(-4) M), whereas picrotoxin (10(-4) M) abolished only the stimulatory phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Kinetic study of melatonin release from rat pineal glands using a perifusion technique.

In previous studies, noradrenaline was found to elicit a rise of melatonin secretion through activation of typical beta-adrenergic receptors. In the present study, a perifusion system was developed to characterize the kinetics of melatonin release from rat pineal glands. Isolated pineal glands from adult male rats were continuously perifused for 15 h in a Krebs-Ringer solution, and the concentration of melatonin in the effluent perifusate was monitored using a specific radioimmunoassay. The rate of release of melatonin declined during the first 3-4 h of perifusion and then remained fairly stable for at least 11 h. The spontaneous release of melatonin was around 20 pg per min and per gland. When pineal glands were stimulated with isoproterenol, melatonin release output linearly increased for at least 2 h after the stimulation. The increase in melatonin release depended on the isoproterenol concentration and on the duration of the stimulation. The analysis of the pattern of melatonin secretion by a single rat pineal gland showed that the secretion was irregular but did not present a clear feature of pulsatile or oscillatory release over a 11 h-long study. The perifusion system was found useful in order to follow the characteristics of melatonin release from pineal glands and should allow investigations of neuronal or hormonal control of pineal gland activities.

Animals↗
PubMed1989

Influence of the central nucleus of the amygdala on the content of corticotropin-releasing factor in the median eminence.

The central nucleus of the amygdala possesses numerous neurons containing corticotropin-releasing factor (CRF). This study demonstrates a striking decrease of the CRF-like immunoreactivity in the median eminence at both 1 and 2 weeks after bilateral lesions of the amygdaloid central nucleus. Lesion of the amygdaloid central nucleus did not alter the neurophysin-like immunoreactivity in the internal zone of the median eminence, indicating the integrity of the efferent neurophysin-containing fibers of the supraoptic and paraventricular hypothalamic nuclei. However, there was a concomitant decrease of neurophysin and CRF-like immunoreactivity in the external zone of the median eminence. These results substantiate the hypothesis that the amygdaloid central nucleus can influence the content of CRF-like material in the median eminence via a multisynaptic pathway involving the synthesis of CRF at the level of the paraventricular nucleus of the hypothalamus. The exact mechanism by which lesion of the amygdaloid central nucleus influences the CRF content in the median eminence remains to be determined.

Amygdala↗