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At least 577 records · Page 32Linked to original sources
PubMed1991

Ca(2+)-independent regulation of neurosecretion by intracellular Na+.

While secretion from nerve endings is strictly controlled by an increase in cytoplasmic free calcium several reports suggest intracellular sodium may serve a regulatory role. Whether sodium acts directly to modulate secretion or indirectly by influencing cytoplasmic calcium dynamics is unknown. This study shows, based on parallel experiments studying [Na+]i, [Ca2+]i and vasopressin secretion, that sodium acts directly to regulate secretion in isolated nerve endings from the rat neurohypophysis. The elevation in secretion that develops is dose-dependently related to the [Na+]i and can occur in the absence of changes in [Ca2+]i.

Animals↗
PubMed1987

Gonadal steroids and neurosecretion: facilitatory influence on LHRH and neuropeptide Y.

Luteinizing hormone releasing hormone (LHRH) is regarded as the primary hypothalamic signal that controls reproduction in the rat. Neuropeptide Y, a recently isolated hypothalamic peptide, appears to regulate LHRH secretion. Our studies show that gonadal steroids act in multiple ways to enhance the neurosecretory functions of each of these neuronal systems and, in addition, they promote excitation by NPY of LHRH release from the hypothalamic nerve terminals.

Animals↗
PubMed1991

'Neurosecretion' by synaptic terminals in the locust corpus cardiacum: is non-synaptic exocytosis part of the regulated or the constitutive pathway?

Nerve fibres form conventional synaptic junctions with gland cells in the corpus cardiacum of the locust, Schistocerca gregaria. They contain synaptic vesicles whose contents are normally electron-lucent, but which react positively to cytochemical tests for amines (eg, incubation in the false transmitter 5-OHDA). Secretory granules are also present in the terminals and such inclusions are known to contain neuropeptides. The granules undergo non-synaptic exocytosis and this process has been visualized by the application of tannic acid. Granule exocytosis gives clear signs of being part of a regulated secretory pathway: it is elevated in vivo by flight--a natural stimulus known to activate the gland (this effect is blocked by prior injection of trehalose); its incidence is closely correlated with a postsynaptic response, suggesting a role for the materials discharged in short-term signalling; and when induced in vitro by high K+, it is Ca(2+)-dependent. However, a low level of exocytosis was encountered under all the conditions employed, suggesting the existence of a constitutive component. It is postulated that the regulated and constitutive patterns of discharge of neuropeptides are related to the roles of these materials as neurotransmitters/modulators and neurotrophic substances, respectively.

Animals↗
PubMed1987

'Neurosecretion' by aminergic synaptic terminals in vivo--a study of secretory granule exocytosis in the corpus cardiacum of the flying locust.

Most nerve terminals forming typical synaptic junctions contain both synaptic vesicles and larger 'secretory granules' with electron-dense contents. Visualization of granule exocytosis from within terminals in the corpus cardiacum is facilitated by injection of tannic acid which immobilizes granule cores as they are discharged. The process of discharge is stimulated by flight-induced activation of the neurones and there is a correlated response by the innervated cells. In contrast to synapses with their vesicle clusters, granule discharge is not targeted upon the postsynaptic cells. These findings have general implications for mechanisms of discharge of neuropeptides and other transmitters from synaptic terminals.

Animals↗
PubMed1987

Influence of the histaminergic system on opiate-induced neurosecretion and behaviour.

The influence of the histaminergic system on fentanyl (Fe)-induced growth hormone (GH) and prolactin (PRL) release as well as on Fe-induced increase of noradrenaline (NA) plasma levels has been studied in male volunteers. These volunteers received, according to a randomized block design, different pretreatments: the H1-antagonist dimethindene (Di) (0.1 mg/kg i.v.), or the H2-antagonist cimetidine (Ci)(5 mg/kg i.v.), or a combination of dimethindene and cimetidine (Di + Ci), or saline. The PRL increase caused by Fe (0.2 mg/70 kg) was not altered by pretreatment with the H1-antagonist Di, the H2-antagonist Ci, or the combination of both. The increase of NA plasma levels after Fe also was not modified by the histamine antagonists. In contrast, the maximum GH increase after Fe was blunted by the combination of Ci and Di, but not by either Ci or Di alone. These results suggest an involvement of the histaminergic system in opiate-induced GH-release.

Adult↗
PubMed1994

The molecular machinery for fast and slow neurosecretion.

Recent studies indicate that the molecular machinery for synaptic vesicle docking and fusion consists of a triad of botulinum/tetanus neurotoxin substrates (synaptobrevin, syntaxin, SNAP-25) that are homologues of proteins required for constitutive secretion. Proposed low-affinity Ca2+ sensors that regulate exocytosis remain to be identified, although recent studies on synaptotagmin suggest that it, along with other proteins, could play this role. Regulated peptide secretion from dense-core granules has been found to utilize a similar machinery for docking/fusion, and recent studies indicate that this pathway involves a pre-docking step that is regulated by a higher affinity Ca2+ sensor.

Animals↗
PubMed2005

A role for the anandamide membrane transporter in TRPV1-mediated neurosecretion from trigeminal sensory neurons.

Many n-acylethanolamines utilize the anandamide membrane transporter (AMT) to gain facilitated access to the intracellular compartment, hence, we hypothesized that this mechanism might be important for anandamide (AEA)- and N-arachidonoyl-dopamine (NADA)-evoked CGRP release from cultured trigeminal ganglion (TG) neurons. Using [14C]AEA we demonstrated that TG neurons transported AEA in a FAAH- and AMT-inhibitable fashion. Although TRPV1-positive TG neurons were found to express fatty acid amide hydrolase, the application of FAAH inhibitors had no effect on AEA-evoked CGRP release. In contrast, application of the AMT inhibitors OMDM-2 or VDM-11 significantly reduced the potency and efficacy of AEA-, NADA- and capsaicin-evoked CGRP release. Moreover OMDM-2 (IC50 values ranging from 6.4-9.6 microM) and VDM-11 (IC50 values ranging from 5.3-11 microM) inhibited CGRP release evoked by EC80 concentrations of AEA, NADA and CAP and these values were consistent with IC50s obtained for inhibition of uptake. OMDM-2 had no effect on CGRP release per se while VDM-11 evoked CGRP release on its own (EC50 approximately 35 microM) in a CPZ-insensitive, but ruthenium red (RR)-sensitive fashion. This is the first demonstration that TG sensory neurons possess an AMT-like mechanism suggesting that this mechanism is important for the pharmacological action of AEA and NADA at native TRPV1 channels.

Amidohydrolases↗
PubMed2004

The multiple actions of black widow spider toxins and their selective use in neurosecretion studies.

The black widow spider venom contains several large protein toxins--latrotoxins--that are selectively targeted against different classes of animals: vertebrates, insects, and crustaceans. These toxins are synthesised as large precursors that undergo proteolytic processing and activation in the lumen of the venom gland. The mature latrotoxins demonstrate strong functional structure conservation and contain multiple ankyrin repeats, which mediate toxin oligomerisation. The three-dimensional structure has been determined for alpha-latrotoxin (alphaLTX), a representative venom component toxic to vertebrates. This reconstruction explains the mechanism of alphaLTX pore formation by showing that it forms tetrameric complexes, harbouring a central channel, and that it is able to insert into lipid membranes. All latrotoxins cause massive release of neurotransmitters from nerve terminals of respective animals after binding to specific neuronal receptors. A G protein-coupled receptor latrophilin and a single-transmembrane receptor neurexin have been identified as major high-affinity receptors for alphaLTX. Latrotoxins act by several Ca(2+)-dependent and -independent mechanisms based on pore formation and activation of receptors. Mutant recombinant alphaLTX that does not form pores has been used to dissect the multiple actions of this toxin. As a result, important insights have been gained into the receptor signalling and the role of intracellular Ca(2+) stores in the effect of alphaLTX.

Animals↗
PubMed2003

Palmitoylation sites and processing of synaptotagmin I, the putative calcium sensor for neurosecretion.

Synaptotagmin I, the calcium sensor for neurotransmission, is palmitoylated. We have identified the palmitoylation sites as five cysteine residues located between the transmembrane and cytoplasmic regions. In contrast to wild-type synaptotagmin, the non-acylated mutant is not converted to the endoglycosidase-H-resistant form after expression in CV-1 cells. This indicates a block in transport through the Golgi complex. However, when expressed in PC-12 and RBL cells non-acylated synaptotagmin is targeted to the plasma membrane and to secretory granules. No significant cleavage of [(3)H]palmitate from synaptotagmin was observed in pulse-chase experiments. This indicates that the majority of fatty acids are structural rather than dynamic components.

Amino Acid Sequence↗