Biomedical subjects

H Vaudry

Publications and source records attributed to H Vaudry.

At least 469 records · Page 26Linked to original sources

PubMed1987

alpha-Melanocyte-stimulating hormone (alpha-MSH) release from perifused rat hypothalamic slices.

A perifusion system was developed to investigate the control of alpha-melanocyte-stimulating hormone (alpha-MSH) release from rat brain. Hypothalamic slices were perifused with Krebs-Ringer bicarbonate (KRB) medium supplemented with glucose, bacitracin and bovine serum albumin. Fractions were set apart every 3 min and alpha-MSH levels were measured by means of a specific and sensitive radioimmunoassay method. Hypothalamic tissue in normal KRB medium released alpha-MSH at a constant rate corresponding to 0.1% of the total hypothalamic content per 3 min. The basal release was not altered by Ca2+ omission in the medium or addition of the sodium channel blocker tetrodotoxin (TTX). Depolarizing agents such as potassium (50 mM) and veratridine (50 microM), which is known to increase Na+ conductance, significantly stimulated alpha-MSH release in a Ca2+-dependent manner. When Na+-channels were blocked by TTX (0.5 microM) the stimulatory effect of veratridine was completely abolished whereas the K+-evoked release was unaffected. These findings suggest that: voltage-dependent sodium channels are present on alpha-MSH hypothalamic neurons; depolarization by K+ induces a marked stimulation of alpha-MSH release; K+- and veratridine-evoke releases are calcium-dependent. Altogether, these data provide evidence for a neurotransmitter or neuromodulator role for alpha-MSH in rat hypothalamus.

Animals↗

PubMed1987

Atrial natriuretic factor (ANF) stimulates the release of alpha-MSH from frog neurointermediate lobes in vitro. Interaction with dopamine, GABA and neuropeptide Y.

The action of atrial natriuretic factor (ANF) on alpha-MSH release from frog neurointermediate lobe was studied in vitro using a perifusion technique. Synthetic ANF Arg101-Tyr 126, at concentrations ranging from 10(-7) to 10(-5)M, caused a dose-related stimulation of alpha-MSH release. In addition, dopamine, GABA and NPY, three neuroendocrine factors which inhibit alpha-MSH secretion totally suppressed the action of ANF on alpha-MSH production. The neural lobe of the amphibian pituitary contains numerous ANF immunoreactive fibers, and this regulatory peptide may diffuse from nerves terminating in the pars nervosa to the pars intermedia. Thus, our results suggest that ANF of hypothalamo-neurohypophysial origin may be involved in the multineuronal regulation of amphibian melanotrophs.

Animals↗

PubMed1987

Melanotropin release inhibiting activity of neuropeptide Y: structure-activity relationships.

We have recently shown that the release of alpha-MSH by the intermediate lobe of the frog pituitary is inhibited by neuropeptide Y (NPY). Using the perifusion technique, we have compared in the present study, the alpha-MSH release inhibiting activities of NPY, various NPY short chain analogues and two other members of the pancreatic polypeptide family, peptide YY (PYY) and avian pancreatic polypeptide (APP). The order of biological potency was NPY greater than NPY[2-36] greater than NPY[16-36] greater than NPY[25-36] greater than NPY[1-15]. Among the two pancreatic polypeptides tested, PYY appeared to be almost as potent as NPY while APP was 6 times less active than NPY. Neither NPY[1-15] nor NPY[16-36] could antagonize the inhibitory effect of NPY on alpha-MSH release. The structure-activity relationship study suggests that the bioactive determinant of NPY is located in the C-terminal part of the molecule.

Animals↗

PubMed1987

The benzodiazepine agonist clonazepam potentiates the effects of gamma-aminobutyric acid on alpha-MSH release from neurointermediate lobes in vitro.

The action of the central-type benzodiazepine-receptor agonist clonazepam on alpha-MSH release has been studied in vitro using perifused frog neurointermediate lobes. High concentrations of clonazepam (3.16 X 10(-5) and 10(-4) M) caused an inhibition of alpha-MSH release and this effect was reversed by the central-type benzodiazepine-receptor antagonist Ro 15-1788. High doses of GABA (10(-5) and 10(-4) M) induced a biphasic effect on pars intermedia cells: a brief stimulation followed by a sustained inhibition of alpha-MSH secretion. Administration of clonazepam (10(-5) M) in the presence of various concentrations of GABA (10(-6) to 10(-4) M) led to a potentiation of both stimulatory and inhibitory phases of alpha-MSH secretion induced by GABA. Ro 15-1788 completely abolished the potentiating effect of clonazepam. Thus our results indicate that endogenous benzodiazepine receptors may modulate the effects of GABA on alpha-MSH secretion.

Animals↗

PubMed1987

Co-distribution of neuropeptide Y and its C-terminal flanking peptide in the brain and pituitary of the frog Rana ridibunda.

By means of the peroxidase-anti-peroxidase technique, the distribution of neuropeptide tyrosine (NPY) and its C-terminal flanking peptide (C-PON) has been studied on serial sections of the brain and pituitary of the frog Rana ridibunda. Throughout the brain, NPY and C-PON-immunoreactive perikarya exhibited a remarkable co-distribution. These two peptides were found to be co-located within the same cell bodies in various brain regions including the dorsal and ventral pallium, the dorsal and ventral infundibular nuclei and the preoptic nucleus. The distribution of NPY- and C-PON-containing fibers in the brain and pituitary was similar. Sequential double immunohistochemical staining using the indirect immunofluorescence method, showed that NPY and C-PON were actually located within the same nerve processes throughout the frog brain and in the intermediate lobe of the pituitary. These studies indicate that the deduced C-PON sequence is present within the frog precursor to NPY and is formed in vivo in the frog brain. Like NPY, C-PON is transported distally in nerve terminals and is likely released with NPY in various regions of the brain and in the intermediate lobe of the pituitary.

Animals↗

PubMed1987

Mapping of neuropeptide Y-like immunoreactivity in the feline hypothalamus and hypophysis.

The distribution of neuropeptide Y (NPY) in the cat hypothalamus and hypophysis was studied with the indirect immunofluorescence technique of Coons and co-workers (Coons, Leduc, and Connolly: J. Exp. Med. 102:49-60, 1955), which provided a detailed map of NPY-like immunoreactive neurons. The immunolabelling was detected in cell bodies, fibers, and terminallike structures widely distributed throughout the whole hypothalamus. A large population of medium-sized NPY-like immunoreactive cell bodies was localized in the area of arcuate nucleus. The number of immunoreactive cell bodies visualized was dramatically increased after intracerebroventricular injections of colchicine. Numerous immunolabelled cell bodies were also visible in the median eminence and scattered in the lateral hypothalamic area. Dense plexuses of NPY-immunoreactive fibers were observed in the arcuate nucleus, internal layer of median eminence, periventricular zone, and paraventricular nucleus. Other regions of hypothalamus displaying numerous NPY-like immunoreactive fibers included dorsal and ventrolateral hypothalamic areas. In contrast, certain hypothalamic areas were almost devoid of NPY-like immunoreactive fibers-namely, the mammillary bodies and suprachiasmatic nucleus. Finally, in neurohypophysis, bright immunofluorescent fibers were observed along the pituitary stalk and penetrating the neural lobe. These results suggest the widespread distribution of the NPY-containing neuronal systems in the cat hypothalamus and hypophysis.

Animals↗

PubMed1987

Immunocytochemical demonstration of proopiomelanocortin- and other opioid-related substances and a CRF-like peptide in the gut of the american cockroach, Periplaneta americana L.

Using the peroxidase-antiperoxidase technique, we showed the presence of peptides which are immunologically resembling mammalian corticotropin releasing hormone (CRF)-, adrenocorticotropic hormone (ACTH)-, beta-endorphin (beta-END)-, alpha-melanocyte stimulating hormone (alpha-MSH)-, methionine-enkephalin (met-ENK)- and leucine enkephalin (leu-ENK)- like immunoreactivity in hundreds to thousands of endocrine cells and nerve fibers in the midgut of the American cockroach Periplaneta americana. In the cockroach hindgut no immunoreactive cell bodies could be observed, although nerve fibers were clearly noticed to be recognized by antisera to CRF, ACTH1-24, ACTH11-24 and beta-END. Nothing is exactly known as to the function(s) of the demonstrated materials, but one can speculate that these numerous immunoreactive cells, might have important paracrine and/or endocrine functions in the insect physiology.

Adrenocorticotropic Hormone↗

PubMed1987

Localization of melanotropin-like peptides in the central nervous system of two insect species, the migratory locust, Locusta migratoria, and the fleshfly, Sarcophaga bullata.

By use of well characterized antisera in the peroxidase-antiperoxidase method, we were able to demonstrate alpha MSH and beta MSH immunoreactive cells and nerve fibres within the nervous system of adults and larvae of Locusta migratoria and 3-, 5- and 8-day-old adult Sarcophaga bullata. In neither of these insect species, any immunoreaction was obtained with a gamma 3MSH-antiserum. Double immunohistochemical stainings revealed that alpha MSH-like and beta MSH-like substances are located in different cells. These cells show no immunoreactivity to a number of antisera against other POMC-derivatives (anti-beta lipotropin, anti beta endorphin, anti-ACTH1-24); thus they appear to contain alpha MSH- or beta MSH-like material in a specific way. The function of the immunologically detected peptides remains to be demonstrated. The distribution of the immunoreactive material suggests that, like in amphibians and other lower vertebrates, the synthesis or release of melanotropins might be under the influence of external stimuli. The present observations support the recently developed concept that even some of the smallest neuropeptides, the melanotropins, have been highly conserved during a long period of evolution.

Animals↗

PubMed1987

Effects of TMB-8 and dantrolene on ACTH- and angiotensin-induced steroidogenesis by frog interrenal gland: evidence for a role of intracellular calcium in angiotensin action.

The influence of intracellular calcium on the steroidogenic response of adrenocortical tissue to ACTH and angiotensin has been studied in the frog, using a perifusion system technique. The release of corticosterone, aldosterone and prostaglandins in the effluent medium was monitored by specific radioimmunoassays. TMB-8 and dantrolene, two potential blockers of calcium mobilization from intracellular pool(s), were tested. Dantrolene (5 X 10(-5) M) significantly reduced basal and angiotensin-induced corticosterone and aldosterone production but had little effect on ACTH-evoked steroid release. Conversely TMB-8 (10(-4) M) profoundly depressed spontaneous as well as ACTH- and angiotensin II-induced corticosteroid secretion, suggesting that this compound may affect not only calcium mobilization from the endoplasmic reticulum pool but also calcium influx. Adrenal glands perifused with both dantrolene and calcium-free medium showed no response to angiotensin II. Conversely, in calcium-free conditions and in the presence of dantrolene, angiotensin II still caused an increase in prostaglandin synthesis. Taken together, these results indicate that 1) dantrolene is a more specific agent than TMB-8 in inhibiting calcium mobilization from intracellular pool(s); 2) ACTH increases corticosteroidogenesis without inducing mobilization of intracellular calcium; 3) angiotensin II stimulates both the efflux of calcium from the endoplasmic reticulum and the influx of calcium through the plasma membrane; 4) calcium is required after prostaglandin production in the steroidogenic response of frog interrenal gland to angiotensin II.

Adrenal Cortex Hormones↗

PubMed1987

Biphasic effect of thyrotropin-releasing factor (TRH) on alpha-melanotropin secretion from frog intermediate lobe in vitro.

The kinetics of alpha-MSH secretion induced by prolonged TRH infusion were studied using perfused frog neurointermediate lobe (NIL). During a 2 h administration of TRH (10(-8) M), the secretion rate of alpha-MSH displayed two phases. During the first phase, secretion of alpha-MSH increased rapidly reaching a maximum within 20 min and then, despite continued TRH infusion, this secretion slowly declined. The second phase was characterized as plateau of elevated release (relative to basal secretion); within this second phase there was often a small peak of released alpha-MSH occurring at about 100 min. Exposure of NIL to another TRH (10(-8) M) pulse 90 min later induced a normal stimulation of alpha-MSH secretion, thus demonstrating the viability of tissue in perifusion. Continuous infusion of cycloheximide (10(-5) M) during a 5 h period totally inhibited the biosynthetic activity of NIL but did not influence TRH-induced alpha-MSH secretion. In particular, cycloheximide had no effect on the second phase of the response to prolonged infusion of TRH. Similarly, during continuous infusion of the monovalent carboxylic ionophore monensin (10(-6) M), the biphasic response to prolonged infusion of TRH (10(-8) M) was still observed. Administration of a short pulse of TRH (10(-7) M) during the declining part of the first phase or during the second phase of prolonged TRH (10(-8) M) infusion induced a significant enhancement of alpha-MSH stimulation. From these results we conclude that prolonged TRH infusion causes alpha-MSH release in a biphasic manner; attenuation of the secretory response to continuous TRH administration does not result from exhaustion of the releasable pool of alpha-MSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Atrial natriuretic factor-like immunoreactivity in the central nervous system of the frog.

The distribution of atrial natriuretic factor-like immunoreactivity in the central nervous system of the frog Rana ridibunda was investigated by indirect immunofluorescence and the immunogold technique, using an antiserum generated in rabbits against synthetic atrial natriuretic factor (Arg 101-Tyr 126). A stereotaxic atlas of neurons containing atrial natriuretic factor-like material was prepared to show the widespread distribution of atrial natriuretic factor-positive cell bodies and fibres in the brain. Appreciable numbers of immunoreactive perikarya were observed in the dorsal and medial pallium, the medial septal nucleus, the anteroventral and ventrolateral areas of the thalamus, the lateral forebrain bundle, the posterocentral and posterolateral thalamic nuclei, the preoptic nucleus, the dorsal infundibular nucleus and the anteroventral tegmental nucleus of the mesencephalon. A heavy accumulation of atrial natriuretic factor-like immunoreactive cell bodies and very dense fibre bundles were noted in the interpeduncular nucleus of the mesencephalon. Fibres were generally seen where cell bodies were observed, particularly in all regions of the pallium and septum nuclei, in the ventral thalamus, the infundibular nucleus and the tegmental area. Moderate numbers of fibres were also noted in several regions where cell bodies were absent, mainly in the amygdala and the infundibular nucleus, the median eminence and most mesencephalic regions. At the electron microscopic level, the immunoreactivity was restricted to dense core vesicles and absent in clear vesicles. These results provide the first evidence for the presence of atrial natriuretic factor in the brain of a non-mammalian chordate. The localization of atrial natriuretic factor-positive material in the frog central nervous system suggests that this peptide may act as a neuromodulator or a neurotransmitter in amphibians.

Animals↗

PubMed1987

Coexistence of melanin-concentrating hormone (MCH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the preoptic nucleus of the frog brain.

Coexistence of MCH- and alpha-MSH-like peptides in specific neurons of the frog hypothalamus has been investigated on serial frozen sections using the indirect immunofluorescence method. In the anterior region of the preoptic nucleus, perikarya containing MCH- and alpha-MSH-immunoreactive materials were co-distributed and the two peptides were generally co-sequestered within the same neurons. In contrast, alpha-MSH immunoreactive neurons of the ventral infundibular nucleus did not contain any MCH-like peptide. These data suggest that MCH and alpha-MSH are transported by the same nerve fibers originating from preoptic perikarya and are likely released together by axon terminals. Since MCH and alpha-MSH exert antagonistic hormonal activities on dermal melanophores, our results suggest that the two regulatory peptides may also interact in the central nervous system.

Animals↗

PubMed1987

Impaired response of growth hormone-releasing hormone (GHRH) measured in plasma after L-dopa stimulation in patients with idiopathic delayed puberty.

In order to investigate the regulation of GH secretion in patients with idiopathic delayed puberty (IDP), either prepubertal (stage P1) or early pubertal (P2), GHRH levels in plasma were measured after stimulation with L-Dopa in a group of 16 patients with IDP. The results were compared to those obtained in 12 patients with constitutional short stature (CSS) at the same stages of puberty, who underwent L-Dopa test for insufficient height. Plasma GHRH levels were measured, after extraction and concentration on C18 Sep Pack columns, by radioimmunoassay using an antibody against 1-40 GHRH, which cross-reacts 100% with 1-44 GHRH. The sensitivity of the assay is 6-8 pg/ml. After L-Dopa intake, the peak of GH was mean +/- SEM 8.6 +/- 1.4 ng/ml in IDP and 12.0 +/- 0.8 ng/ml in CSS (NS). The peak of GHRH after L-Dopa was 41 +/- 10 pg/ml in IDP and 96 +/- 25 pg/ml in CSS (p less than 0.02). A significant (p less than 0.02) decrease of plasma GHRH peak values (mean +/- SEM 17.3 +/- 4.4 pg/ml) was noted in the five patients with IDP whose growth velocity was below -2 SD for their bone age compared to the patients with normal growth velocity (mean +/- SEM 75.0 +/- 14.5 pg/ml). These results suggest a hypothalamic dysfunction in patients with IDP, and a relationship between the well-known partial and transitory somatotropic deficiency found in some adolescents having a pubertal delay and their secretion of the releasing hormone GHRH.

Adolescent↗

PubMed1987

Characterization of gamma-aminobutyric acid receptors in the neurointermediate lobe of the amphibian Xenopus laevis.

The neurotransmitter gamma-aminobutyric acid (GABA) is involved in the regulation of secretion of MSH from the intermediate lobe of Xenopus laevis. The purpose of this study was to identify the GABA receptor(s) involved by determination of the effect of specific receptor agonists and antagonists on the release of immunoreactive MSH from superfused neurointermediate lobes of Xenopus. Exogenous GABA induces a rapid inhibition of MSH secretion. There was no evidence for a transitory stimulatory effect of GABA as reported for the rat melanotropes. Both the GABA agonists (GABAa) homotaurine and isoguvacine and the GABA agonist (GABAb) baclofen inhibited MSH release in a dose-dependent manner. In vivo, homotaurine and baclofen caused aggregation of pigment in dermal melanophores. The MSH release-inhibiting effect of homotaurine and isoguvacine could be antagonized by the specific GABAa receptor antagonist bicuculline. However, bicuculline and picrotoxin failed to block the effect of exogenous GABA. We conclude that in the neurointermediate lobe of Xenopus laevis both GABAa and GABAb receptors are present, suggesting a dual inhibitory regulation.

Animals↗

PubMed1987

Acetylcholine stimulates steroidogenesis in isolated frog adrenal gland through muscarinic receptors: evidence for a desensitization mechanism.

The effect of cholinergic agonists on glucocorticoid and mineralocorticoid production by frog interrenal (adrenal) tissue was studied in vitro by means of continuous perifusion. Acetylcholine, at doses ranging from 1 to 100 mumol/l, stimulated both corticosterone and aldosterone output in a dose-dependent manner, with a half-maximal effective dose of 2.5 mumol/l. Corticosteroid production was also stimulated by muscarine (10 mumol/l). In contrast, neither nicotine nor nicotine bitartrate (1-100 mumol/l) enhanced corticosteroid biosynthesis. The kinetics of the response of adrenal cells to acetylcholine and muscarine were similar to those observed during angiotensin II stimulation. In particular, a significant reduction (20-40%) in the spontaneous level of corticosteroid production was recorded after the initial infusion of muscarinic agents, but no further decrease in the basal level occurred after a second cholinergic administration. The effect of acetylcholine was blocked by the muscarinic receptor antagonist atropine (10 mumol/l). These results indicate that acetylcholine can stimulate frog adrenocortical cells through muscarinic receptors. Repeated 20-min pulses of acetylcholine (50 mumol/l) or muscarine (10 mumol/l), given at one pulse per 130 min, resulted in a marked reduction in the secretory response to the second pulse. No reduction in the stimulatory effect of acetylcholine or muscarine was observed when a 6.5-h interval separated two 20-min infusions of the secretagogue. In contrast with these findings, iterative pulses of the muscarinic agonist pilocarpine (in the range 1-100 mumol/l) did not cause any desensitization. These data show that the neurotransmitter acetylcholine can modulate frog adrenocortical function and suggest that, in addition to more conventional regulators, i.e. ACTH and angiotensin II, the cholinergic endings of the splanchnic nerve might participate in the regulation of corticosteroid secretion, at least under some physiological conditions such as neurogenic stress.

Acetylcholine↗

PubMed1987

[Role of microtubules in adrenal gland steroidogenesis].

In order to determine the role of the microtubular network in adrenal steroidogenesis, we have studied the effect of vinblastine, a potent antimicrotubular agent on corticosteroid secretion by frog adrenocortical fragments in perifusion. Administration of vinblastine (10(-5) M) did not alter the spontaneous secretion of corticosteroids and had no effect on the steroidogenic response to angiotensin II and prostaglandin E1. In contrast, vinblastine induced a marked decrease in ACTH-induced stimulation of corticosteroidogenesis. To investigate further the site of action of the microtubular system in ACTH-induced steroidogenesis we have studied the effect of vinblastine on the different steps of the stimulation of the adenylate cyclase system. Our results show that vinblastine does not alter the stimulatory action of cAMP, the second messenger of ACTH. In addition, the corticosteroidogenic effect of forskolin and NaF (which respectively stimulate the adenylate-cyclase subunit and the guanyl nucleotide regularly protein) was not affected by vinblastine. These results indicate that the microtubular network interferes in the coupling of the secretory response of the adrenal glands to ACTH, either at the level of the binding of ACTH to its receptor or in the coupling of the receptor to the guanyl nucleotide regulatory protein.

Adrenal Cortex Hormones↗

PubMed1987

[Pro-opiomelanocortin neuronal systems].

Proopiomelanocortin (POMC) is a glycoprotein which serves as a multihormonal precursor for corticotropin (ACTH), lipotropins (beta and gamma-LPH), melanotropins (alpha, beta- and gamma-MSH) and endorphins (alpha-, beta- and gamma-endorphins). This precursor protein is primarily synthesized in corticotrophs of the anterior lobe and in melanotrophs of the intermediate lobe of the pituitary, as well as in other organs or tissues such as the genitourinary tract, the gastrointestinal tract and leukocytes. POMC is also present in the central nervous system (CNS) and numerous studies have been conducted to determine the localization, biosynthesis and functions of POMC-derived peptides. The identification of POMC-neuronal systems has been achieved by combining immuno histochemical studies, biochemical analysis, bioassays and radioimmunoassays. Three groups of perikarya containing various POMC-related peptides have been identified. One of these is located in the arcuate nucleus in the basal hypothalamus and projects towards the septum, thalamus and telencephalon. Some fibers originating from the arcuate nucleus terminate in the nucleus of the solitary tract in the brainstem where a second group of POMC-containing nerve cells are located. The latter innervates both the mesencephalon, the brainstem and the spinal cord. A third group of neurons, which contain alpha-MSH but not other POMC-derivates, has been identified in the zona incerta in the dorso-lateral hypothalamus. Processing of POMC in the cell bodies of the arcuate nucleus follows a similar pattern as in the pituitary intermediate lobe. Endopeptidases called "acid-thiol-arginyl-proteases" cleave the prohormone at paired basic amino acids. The basic residues remaining on the resulting peptides are subsequently eliminated by the joint action of the less specific B-type carboxypeptidases and B-type aminopeptidases. alpha-MSH and beta-endorphin are among the major end products. Enzymatic modifications including N-alpha-acetylation by opiomelanotropin-acetyltransferase (OMAT) and/or C-terminal amidation by peptidyl-glycine alpha-amidating monooxygenase (PAM) occur after proteolytic processing. However, the rate of acetylation observed in hypothalamic POMC neurons is much lower than in the melanotrophs of the pars intermedia. Acetylation of MSH and endorphin is crucial in determining the biological potency of these peptides. Desacetyl alpha-MSH is far less active than alpha-MSH (monoacetyl alpha-MSH), whereas acetylated beta-endorphin has no opiate activity. The mechanisms regulating the activity of POMC-containing neurons are still unknown.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1986

Localization of atrial natriuretic factor (ANF)-immunoreactive material in the hypothalamo-pituitary complex of the frog.

The presence of atrial natriuretic factor (ANF)-like material in the hypothalamo-pituitary complex of the frog (Rana ridibunda) was studied by means of indirect immunofluorescence and immunogold techniques. In the hypothalamus, numerous ANF-positive cell bodies were located in the preoptic nucleus, the lateral forebrain bundle and the dorsal infundibular nucleus. The ventral infundibular area and the median eminence contained only ANF-immunoreactive fibers. A dense network of fibers and nerve terminals was observed in the neural lobe of the pituitary. Scarce nerve endings were also noted in the intermediate lobe whereas ANF-like immunoreactivity was totally absent in the anterior lobe of the pituitary. At the ultrastructural level, positive material appeared restricted to dense core vesicles (about 100 nm in diameter). These results demonstrate that an ANF-like substance is contained in nerve terminals of the frog pars nervosa, and support the hypothesis that ANF may exert a physiological role in the control of release of neurohypophyseal peptides.

Animals↗