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PubMed1999

Neurosecretory cells without neurosecretion: evidence of an independently regulated trait of the cell phenotype.

Neurosecretion competence is a fundamental property that enables differentiated neurones and professional neurosecretory cells to store neurotransmitters and hormones in specialized organelles, the synaptic-like vesicles and dense granules, and to release them by regulated exocytosis. In our laboratory, the study of rat phaeochromocytoma (PC12) clones that fail to express the above organelles or any other components involved in neurosecretion, whilst maintaining most of the general markers of the parental population, has served to demonstrate that this trait is controlled independently from the rest of the phenotype. The present review focuses on recent advances in elucidating the molecular mechanisms governing neurosecretion competence. Moreover, the opportunities that such neurosecretion-defective PC12 clones offer for the investigation of new aspects of regulated exocytosis and the localization of its components are summarized.

Animals↗

PubMed1992

Ca(2+)-independent and Ca(2+)-dependent stimulation of quantal neurosecretion in avian ciliary ganglion neurons.

1. Although it is generally agreed that Ca2+ couples depolarization to the release of neurotransmitters, hypertonic saline and ethanol (ETOH) evoke neurosecretion independent of extracellular Ca2+. One possible explanation is that these agents release Ca2+ from an intracellular store that then stimulates Ca(2+)-dependent neurosecretion. An alternative explanation is that these agents act independently of Ca2+. 2. This work extends previous observations on the action of ETOH and hypertonic solutions (HOSM) on neurons to include effects on [Ca2+]i. We have looked for Ca(2+)-independent or -dependent neurosecretion evoked by these agents in parasympathetic postganglionic neurons dissociated from chick ciliary ganglia and maintained in tissue culture. The change in concentration of free Ca2+ in the micromolar range inside neurons ([Ca2+]i) was measured with indo-1 with the use of a Meridian ACAS 470 laser scanning microspectrophotometer. 3. Elevated concentration of extracellular KCl increased [Ca2+]i and the frequency of quantal events. Also, a twofold increase in osmotic pressure (HOSM) produced a similar increase in quantal release and a significant rise in [Ca2+]i; however, the Ca2+ appeared to come from intracellular stores. 4. In contrast, ETOH stimulated quantal neurosecretion without a measurable change in [Ca2+]i. It appears the alcohol exerts its influence on some stage in the process of exocytosis that is distal to or independent of the site of Ca2+ action. 5. The effects of high [KCl]o and osmotic pressure were occlusive. This is explained in part by the observation that hypertonicity reduced Ca2+ current, but an action on Ca2+ stores is also likely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Stochastic modeling of facilitated neurosecretion.

Two models of neurosecretion were evaluated in terms of their ability to predict the dependency of quantal content (m) on the frequency of repetitive stimulation of a lobster motoneuron. First, the hypothesis that neurosecretion is limited by a fixed number of release sites was tested by the fit of the distribution of m by uniform and nonuniform binomial statistics. The obtained release probabilities suggest that frequency facilitation can be due to activation of a group of sites with high release probabilities. However, the fit obtained using this model is not statistically significant due to a large number of fitting parameters. Second, the hypothesis that neurosecretion is limited by the rates of exchange between the releasable pool and the total store of quanta and that each stimulus enhances quantal mobilization was tested. Monte Carlo simulation was carried out in accordance with this model and reproduced the observed distribution of m with very few fitting parameters and therefore with a high level of significance (>0.1). This result demonstrates that mobilization of extra vesicles with each stimulus is a mechanism that allows a very accurate and parsimonious quantitative description of frequency facilitation.

Action Potentials↗

PubMed1999

Oxidative stress and a murine superoxide dismutase-1 mutation promoting amyotrophic lateral sclerosis alter neurosecretion in the hypothalamo-neurohypophyseal axis.

In this study, we examined the effects of oxidative stress on a nitric oxide (NO)-regulated neuroendocrine function, the release of arginine vasopressin (AVP) by the hypothalamo-neurohypophyseal axis. Treatment of mouse-isolated hypothalami and neurointermediate lobes (NIL) with H2O2 increased AVP release. This effect was inhibited by copper-zinc superoxide dismutase-1 (SOD1) analogs. By measuring cGMP accumulation as an indicator of biologically active NO, we found that H2O2 treatment decreased cGMP formation in both hypothalami and NIL. We have previously shown that NO inhibits AVP release by a cGMP-independent mechanism. Given that H2O2 stimulated AVP release, while it reduced cGMP production, our findings strongly suggest that oxidative damage affects neurosecretion by reducing NO availability. To test whether such a mechanism may operate under pathological conditions with pronounced oxidative stress, we compared neurosecretion in wild-type and transgenic mice carrying a mutated form of SOD1 associated with human familial amyotrophic lateral sclerosis. Reminiscent of the data obtained from H2O2-treated tissues, hypothalami and NIL from SOD1 mutants displayed decreased cGMP accumulation and increased AVP release, compared with tissues from wild-type littermates. Since neuronal NO synthase expression was not modified, we conclude that the perturbed free radical metabolism associated with the SOD1 mutation is likely to trap NO, and thereby alter neurosecretion, a mechanism that can be exacerbated in specific physiopathological conditions.

Amyotrophic Lateral Sclerosis↗

PubMed1979

[Experimental hepatic encephalopathy. The effect of portocaval shunt on the evolution of the anterior hypothalamic neurosecretion in the rat (author's transl)].

The evolution of the anterior hypothalamic neurosecretion is studied in control, sham-operated and portocaval shunt rats. In sham-operated related to control rats, no modification of the anterior hypothalamic neurosecretion is observed. In portocaval shunt rats, the hypothalamic neurosecretion increases. This increase is mainly observed into the median eminence in all the portocaval shunt rats. The hypothesis according to which the modification of neurosecretory acitivity of the hypothalamic structures may be related to a discrepancy between the central monoamines is discussed.

Animals↗

PubMed2003

Contributions of insect research toward our understanding of neurosecretion.

The process of neurosecretion is an important and widespread method of biological communication among animals. Although insects and vertebrates appear to be very different, neurosecretory mechanisms and the neuropeptides themselves are often the same. The gradual acceptance of neurosecretion as a biological phenomenon, largely as a result of research done with insects, is discussed.

Animals↗

PubMed1978

Histopathology and histochemistry of the insects treated with chemosterilants VI: brain damage including reduced neurosecretion caused by chemosterilants in Periplaneta americana (L).

The brain is damaged and neurosecretion is reduced in the P. americana treated with chemosterilants thio-tepa and bis (dimethylamino) dithiazolium chloride. The damage includes, separation of neurolemma, vacuolisation and chromatolysis in the nuclei of neurons and extensive damage to fibres. Reduced neurosecretion, vacuolisation in the cytoplasm and karyolysis in the nucleus of neurosecretory cells, are also observed. These changes in the brain are of considerable importance to understand the mode of action of the chemosterilants.

Animals↗

PubMed1998

Neurosecretion competence, an independently regulated trait of the neurosecretory cell phenotype.

Neurosecretion competence is intended as the ability of neurosecretory cells to express dense and clear vesicles discharged by regulated exocytosis (neurotransmitter release). Such a property, which so far has never been studied independently, is investigated here by a heterotypic cell fusion approach, using a clone of rat pheochromocytoma PC12 cells totally incompetent for neurosecretion that still largely maintains its typical molecular and cellular phenotype. When fused with wild-type partners of various species (rat, human) and specialization (PC12, neuroblastoma SH-SY5Y, HeLa), the defective cells reacquire their competence as revealed by the expression of their secretion-specific proteins. Fused wild-type cells therefore appear able to complement defective cells by providing them with factor(s) inducing the reactivation of their secretory program. The mechanism of action of these factors may consist not in a coordinate unblocking of transcription but in the prevention of a rapid post-transcriptional degradation of the mRNAs for secretion-specific genes.

Animals↗

PubMed2006

Localization of synaptic proteins involved in neurosecretion in different membrane microdomains.

A number of proteins and signalling molecules modulate voltage-gated calcium channel activity and neurosecretion. As recent findings have indicated the presence of Ca(v)2.1 (P/Q-type) channels and soluble N-ethyl-maleimide-sensitive fusion protein attachment protein receptors (SNAREs) in the cholesterol-enriched microdomains of neuroendocrine and neuronal cells, we investigated whether molecules known to modulate neurosecretion, such as the heterotrimeric G proteins and neuronal calcium sensor-1 (NCS-1), are also localized in these microdomains. After immuno-isolation, flotation gradients from Triton X-100-treated synaptosomal membranes revealed the presence of different detergent-resistant membranes (DRMs) containing proteins of the exocytic machinery (Ca(v)2.1 channels and SNAREs) or NCS-1; both DRM subtypes contained aliquots of heterotrimeric G protein subunits and phosphatidylinositol-4,5-bisphosphate. In line with the biochemical data, confocal imaging of immunolabelled membrane sheets revealed the localization of SNARE proteins and NCS-1 in different dot-like structures. This distribution was largely impaired by treatment with methyl-beta-cyclodextrin, thus suggesting the localization of all three proteins in cholesterol-dependent domains. Finally, bradykinin (which is known to activate the NCS-1 pathway) caused a significant increase in NCS-1 in the DRMs. These findings suggest that different membrane microdomains are involved in the spatial organization of the complex molecular network that converges on calcium channels and the secretory machinery.

Animals↗

PubMed2005

The role of Snapin in neurosecretion: snapin knock-out mice exhibit impaired calcium-dependent exocytosis of large dense-core vesicles in chromaffin cells.

Identification of the molecules that regulate the priming of synaptic vesicles for fusion and the structural coupling of the calcium sensor with the soluble N-ethyl maleimide sensitive factor adaptor protein receptor (SNARE)-based fusion machinery is critical for understanding the mechanisms underlying calcium-dependent neurosecretion. Snapin binds to synaptosomal-associated protein 25 kDa (SNAP-25) and enhances the association of the SNARE complex with synaptotagmin. In the present study, we abolished snapin expression in mice and functionally evaluated the role of Snapin in neuroexocytosis. We found that the association of synaptotagmin-1 with SNAP-25 in brain homogenates of snapin mutant mice is impaired. Consequently, the absence of Snapin in embryonic chromaffin cells leads to a significant reduction of calcium-dependent exocytosis resulting from a decreased number of vesicles in releasable pools. Overexpression of Snapin fully rescued this inhibitory effect in the mutant cells. Furthermore, Snapin is relatively enriched in the purified large dense-core vesicles of chromaffin cells and associated with synaptotagmin-1. Thus, our biochemical and electrophysiological studies using snapin knock-out mice demonstrate that Snapin plays a critical role in modulating neurosecretion by stabilizing the release-ready vesicles.

Animals↗

PubMed2001

Nicotinic acid adenine dinucleotide phosphate enhances quantal neurosecretion at the frog neuromuscular junction: possible action on synaptic vesicles in the releasable pool.

Inositol 1,4,5-trisphosphate (IP(3)) and cyclic adenosine diphosphate-ribose (cADPR) are second messengers that enhance neurosecretion by inducing Ca(2+) release from smooth endoplasmic reticulum (SER). The putative intracellular messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), releases Ca(2+) from stores that are distinct from SER. Evidence is presented here that NAADP causes a concentration-dependent increase in quantal output that is associated with an increase in probability of transmitter release at the frog neuromuscular junction. This effect is mimicked by A23187, a Ca ionophore that promotes Ca(2+) entry at the plasmalemma. The response to NAADP is potentiated by IP(3) but antagonized by cADPR. Thapsigargin completely blocks IP(3) and cADPR responses and decreases but does not prevent the response to NAADP. We conclude that NAADP, whose receptors are widely distributed in the brain, enhances neurosecretion by releasing Ca(2+) from an internal store near the plasmalemma, possibly from synaptic vesicles in the releasable pool. These data also support the hypothesis of a two-pool model for Ca(2+) oscillations at the presynaptic site.

Adenosine Diphosphate Ribose↗

PubMed1975

[Distribution of neurosecretion in the neurohypophysis of the cow during and following milking].

Studies by optical microscopy showed that discharge of neurosecretion brought about by the stimulus of milking took place in the zona centralis and also in the transitional and main sectors of the zona terminalis. The zona marginalis, zona metacentralis and the peripheral sector of the zona terminalis were not involved. In pituitary glands fixed at various time intervals after milking, the increase in secretion content and the disappearance of perivascular accumulations of secretion were evidently a result of renewed production and storage of neurosecretion in the hypophysis. The renewed homogeneous distribution of secretion in the zona terminalis had not been completed one hour after milking. The increase in size and number of pituicytes and their frequent appearance in adventitious tissue of vessels and around sinusoid capillaries after the liberation of secretion may be related to degradation processes of neurosecretory material.

Animals↗

PubMed1981

Neurosecretion of the hypothalamo-hypophyseal system after intragastric administration of zinc oxide.

Considering the importance of Zn for normal metabolic processes as well as its neurotoxic properties when ingested in undue amounts we have undertaken a study on the effect of ZnO intoxication on the neurosecretory function of the hypothalamus and hypophysis. The investigations were performed on rats that have been treated intragastrically with ten daily (100 mg) doses of ZnO. The intoxicated rats revealed elevated contents of neurosecretion in the neurosecretory nuclei of the hypothalamus along with decline amounts of neurosecretion in the nervous parts of the hypophysis. The contents of PAS-positive substances was increased all over the neurosecretory hypothalamo-hypophyseal system. The concurrent enlargement of the nuclear and cytoplasmatic areas of the secreting cells speaks in favour of the conclusion that the observed histochemical and morphometric alterations reflect both an increased neurosecretory activity of the hypothalamus and in enhanced release of antidiuretic hormone.

Animals↗

PubMed1980

Neurosecretion in the milkweed bug, Lygaeus pandurus scop. (Heteroptera: Lygaeidae).

Neurosecretory cells in the brain, ventral ganglia, and retrocerebral endocrine glands aortal complex of a milkweed bug, Lygaeus pandurus Scop. have been described using a variety of techniques in whole mounts and sections. Two main types of neurosecretory cells viz. A and B types, have been distinguished on the basis of histochemical and staining properties. The A-type of cells have been further divided into 4-sub types viz. A-1, A-2, A-3 and A-4 on the basis of staining properties and cell size. There are only one type of B-cells. The brain and all the ventral ganglia contain neurosecretory cells including the frontal ganglion. The brain consists of A-1, A-2 and B-cells, the suboesophageal and prothoracic ganglia have A-2, A-3 and B-cells, and the lat ganglion have A-2 and B-cells. The frontal ganglion contains only A-4 type of cells. The corpora cardiaca are ovoid bodies consisting of large and small chromophil cells. The chromophil cells are positive to PF and PARF but negative to PAVB. In addition to the secretions of the chromophil cells, the gland also acts as storage organ for lateral, ventral, posterior and anterior neurosecretions of the brain. The corpus allatum which is an unpaired globular epitheloid body, lies behind the corpora cardiaca. It consists of one type of cells. The gland is devoid of A-1 cell NSM i.e. Victoria blue positive material. At times, it shows a small amount of A-2 cell NSM. The aorta which receives the axons of NCC-I is provided with a large amount of neurosecretory material, elaborated in the medial neurosecretory cells of the brain. Thus, in Lygaeus pandurus aorta and not the CC, functions as NHO for medial neurosecretions.

Animals↗

PubMed1988

Peripubertal development of noradrenergic stimulation of luteinizing hormone-releasing hormone neurosecretion in vitro.

The effect of age on norepinephrine (NE) stimulation of luteinizing hormone-releasing hormone (LH-RH) secretion from preoptic area-mediobasal hypothalamic (POA-MBH) explants was examined in the present study. Explants were obtained from juvenile (9-day-old), prepubertal (29-day-old) and adult female rats. Following decapitation and surgical isolation, POA-MBH explants were individually perifused with culture medium which was collected for radioimmunoassay of LH-RH. Explants were exposed to two pulses of medium containing NE (5 x 10(-4) M, peak concentration) and a terminal pulse of medium containing KCl (45 mM, peak concentration) for assessment of viability. POA-MBH explants obtained from prepubertal female rats exhibited increased LH-RH release in response to the two pulses of NE and subsequent KCl pulse (P less than 0.05). NE was without effect in stimulating LH-RH neurosecretion from POA-MBH explants obtained from 9-day-old female rats although these explants were responsive to KCl (P less than 0.01). Two-day pretreatment of 9-day-old, and prepubertal rats with estradiol benzoate (EB) did not alter the LH-RH response to this dose of NE or KCl (no group or interaction effects) in prepubertal female rat explants and did not render the explants from 9-day-old rats responsive to NE. Furthermore, NE was equally effective in stimulating LH-RH release from explants obtained from estradiol-treated or control ovariectomized adult rats. These observations demonstrate a peripubertal activation of the stimulatory effect of NE on LH-RH release from POA-MBH explants in vitro. Although these data also suggest that estrogen is not obligatory for NE stimulation of LH-RH release from POA-MBH explants, further investigation is required to determine the developmental time course and estrogen dependency of the noradrenergic stimulation of LH-RH neurosecretion and to evaluate whether estrogen alters the sensitivity of POA-MBH explants to lower concentrations of NE as has been previously reported for median eminence fragments.

Animals↗

PubMed1986

Hormones, neurosecretions, and growth factors as signal molecules for intercellular communication.

Chemical signals, whether in the form of hormones, neurosecretions (neurotransmitters and neuropeptides), or growth factors and chalones are used to communicate information to cells at all stages of their life cycle. These signals inform the cells when it is time to progress through developmental change, when to change the rates of various activities (e.g. metabolism or contraction), and, in some cases, even when it is time to die. Throughout all of these interactive exchanges, the signal molecule itself carries no intrinsic message of a universal nature. The chemical identity of the signal molecule has meaning only for those cells competent to receive the signal (i.e. does it possess an appropriate receptor?). Moreover, it is the nature of the cell receiving the signal (itself the product of innumerable previous encounters with signals from other cells) that dictates the specific response that a particular signal will evoke. The signal emitted by the communicating cell only informs the target cell that it is time to act in a manner consistent with that signal. The majority of the discussion has been from the perspective of vertebrate organisms. Moreover, of necessity, the discussion has been general and superficial. The primary objective of the preceding discussion has been to underscore major similarities and differences existing among hormones, neurosecretions (neurotransmitters and neuropeptides), and growth factors as information-bearing substances used in communication among vertebrate cells. It should be realized that similar means of communication are employed by multicellular invertebrates, by plants, and even by single-celled organisms such as the protists and bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Communication↗

PubMed2004

Human growth hormone co-transfection assay to study molecular mechanisms of neurosecretion in PC12 cells.

The recent introduction of transient co-transfection assays, with human growth hormone (hGH) as a marker of transfection, has allowed us to study the function of transfected proteins in neurosecretion using intact PC12 cells and adrenal chromaffin cells [J. Biol Chem. 268 (1993) 10983]. Since this assay requires several non-trivial steps (transfection of the genes, triggering of secretion, and measurement of hGH), care should be taken before attributing any observed effect to the transfected proteins. In this article, we describe a detailed procedure for the hGH transfection assay and show that this approach can be used to study the molecular events involved in neurosecretion.

Animals↗

PubMed2002

Neurosecretion competence. A comprehensive gene expression program identified in PC12 cells.

The phenotype of neurosecretory cells is characterized by clear vesicles and dense granules, both discharged by regulated exocytosis. However, these organelles are lacking completely in a few neurosecretion-incompetent clones of the pheochromocytoma PC12 line, in which other specific features are maintained (incompetent clones). In view of the heterogeneity of PC12 cells, a differential characterization of the incompetent phenotype based on the comparison of a single incompetent and a single wild-type clone would have been inconclusive. Therefore, we have compared two pairs of PC12 clones, studying in parallel the transcript levels of 4,200 genes and 19,000 express sequence tags (ESTs) by high density oligonucleotide arrays. After accurate data processing for quality control and filtration, a total of 755 transcripts, corresponding to 448 genes and 307 ESTs, was found consistently changed, with 46% up-regulated and 54% down-regulated in incompetent versus wild-type clones. Many but not all neurosecretion genes were profoundly down-regulated in incompetent cells. Expression of endocytosis genes was normal, whereas that of many nuclear and transcription factors, including some previously shown to play key roles in neurogenesis, was profoundly changed. Additional differences appeared in genes involved in signaling and metabolism. Taken together these results demonstrate for the first time that expression of neurosecretory vesicles and granules is part of a complex gene expression program that includes many other features that so far have not been recognized.

Animals↗