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PubMed2000

Molecular analysis of vesicular amine transporter function and targeting to secretory organelles.

Vesicular transporters are responsible for the loading of neurotransmitters into specialized secretory organelles in neurons and neuroendocrine cells to make them available for regulated neurosecretion. The exocytotic release of neurotransmitter therefore depends on the functional activity of the vesicular transporters and their efficient sorting to these secretory organelles. Molecular analysis of vesicular transport proteins has revealed important information regarding structural domains responsible for their functional properties, including substrate specificity and trafficking to various classes of secretory vesicles. These studies have established the existence of an important functional relationship between transporter activity and presynaptic quantal neurosecretion.

Amines↗
PubMed1985

Rapid sequestration and degradation of somatostatin analogues by isolated brain microvessels.

Somatostatin (SRIF) is a putative peptide neurotransmitter that may interact with brain capillaries following neurosecretion of the peptide. The present studies investigate the binding and metabolism of SRIF analogues in isolated bovine brain microvessels. 125I-[Tyr1]SRIF was rapidly degraded by capillary aminopeptidase with a half-time of approximately 3 min at 23 degrees C. The microvessel aminopeptidase had a low affinity and high capacity for the peptide, Km = 76 microM and Vmax = 74 nmol min-1 mgp-1. 125I-[Tyr11]SRIF was converted to free iodotyrosine at a much slower rate, presumably by a lower-activity endopeptidase. 125I-[Try11]SRIF was rapidly bound by microvessels, whereas another basic peptide, [Tyr8]bradykinin, or an acidic peptide, CCK8, or a neutral peptide, leucine enkephalin, were bound to a considerably less extent. The binding of 125I-[Tyr11]SRIF to the capillaries was nonsaturable up to a concentration of 1 microgram/ml of unlabeled peptide, and the binding reaction was extremely rapid, reaching equilibrium within 5 s at either 0 degrees C or 37 degrees C. Approximately 20% of the SRIF bound by the microvessels was resistant to acid wash and presumably represented internalized peptide. In addition, the 125I-[Tyr11]SRIF bound rapidly to the endothelial cytoskeleton remaining after a 1% Triton X-100 extraction of the microvessels. The peptide-cytoskeletal binding reaction was nonsaturable up to 1 microgram/ml of unlabeled [Tyr11]SRIF, but it was inhibited by 0.5% polylysine or 0.8 M KCl and was stimulated by 1 mM dithiothreiotol. These studies suggest that brain microvessels rapidly sequester and degrade SRIF analogues and that this may represent one mechanism for rapid inactivation of the neuropeptides subsequent to neurosecretion.

Aminopeptidases↗
PubMed1990

The problem with autoreceptors.

There are numerous problems with the concept that antagonists enhance transmitter release by blockade of feedback. It was shown that antagonist enhancement of transmitter release does not correlate satisfactorily with the intensity of stimulation or with other indices of biophase transmitter concentration. Wide variations were shown to exist between antagonists in the amount of enhancement of release they induce. Also, antagonists enhance transmitter release or the effector response with a single stimulation pulse, a condition under which no feedback is possible. A study of agonist/antagonist relationships indicates different sites of action, and it was determined that the antagonist effect has negligible or minimal latency and that enhancement by antagonists is maximal under minimal condition of stimulation. Antagonists were shown to enhance release by a direct action, not by passive occupancy of agonist sites. Experiments were described in which acetylcholine and cold selectively antagonized antagonist but not agonist effects. Further, experiments with pulse duration shifts and with veratridine pointed to a direct action of antagonists on Na+ (also Ca++?) channel gating mechanisms, which results in a shift in the voltage dependence of activation. If antagonists, in some particular instances, enhance release by blockade of sites involved in negative feedback this is likely lost or mired in their more prominent direct actions on neurosecretion--and these must be sorted out. The acceptance of the fact that antagonists act directly to alter transmitter release (and not only as passive occupiers of presynaptic receptors), as the present study shows, both in the central nervous system and in the periphery, opens a new area for future investigation, and may be exploitable for therapeutic purposes and to gain an enriched understanding of the mechanism of neurosecretion.

Adrenergic alpha-Antagonists↗
PubMed2005

Expression of native alpha3beta4* neuronal nicotinic receptors: binding and functional studies investigating turnover of surface and intracellular receptor populations.

Several pathological conditions involve alterations in expression of neuronal nicotinic acetylcholine receptors (nAChRs). Although some studies have addressed processes involved with muscle nAChR expression, knowledge of the regulation of neuronal nAChRs is particularly sparse. The following studies were designed to investigate cellular mechanisms involved with expression of neuronal alpha3beta4* nAChRs. Catecholamine secretion assays and receptor binding studies coupled with receptor alkylation were used to study the nAChR regulation and turnover. Alkylation of adrenal nAChRs results in a rapid and complete loss of receptor-mediated neurosecretion and surface [(3)H]epibatidine binding sites. After alkylation, both neurosecretory function and nAChR binding slowly (24-48 h) return to prealkylation levels. When cells are treated with the protein synthesis inhibitor puromycin, after alkylation, receptor-mediated neurosecretion does not recover. Long-term treatment (24-48-h) with puromycin, in the absence of alkylation, results in a slow, time-dependent shift to the right, followed by a downward shift, in the nicotine concentration-response curve, documenting a disappearance of surface nAChRs. Puromycin treatment alone also results in a loss to both surface and intracellular [(3)H]epibatidine binding sites. nAChR beta4 subunit levels are significantly decreased after treatment with puromycin. These data support a constitutive turnover of adrenal alpha3beta4* nAChRs, requiring continual de novo synthesis of new receptor protein.

Animals↗
PubMed2000

Prostaglandin E2 enhances bradykinin-evoked iCGRP release in bovine dental pulp.

Mediators produced during inflammation are responsible for hyperalgesia and expression of neurotransmitters and receptors in the nervous system. The production of bradykinin (BK) and the prostaglandins (PGs) may regulate initiation of pain. This study tested the hypothesis that BK and prostaglandin E2 (PGE2) have a positive interaction in evoking neurosecretion of immunoreactive calcitonin gene-related peptide (iCGRP). Bovine dental pulp was prepared and stimulated by the superfusion method with BK alone and in combination with PGE2. Kinin receptor antagonists to bradykinin-evoked release of iCGRP were also tested. Also tested was the hypothesis that dental pulp contains either the B1 or B2 or both BK receptors. Results showed that PGE2 enhanced BK-evoked iCGRP release by more than 50%. Western immunoblots revealed detectable B2 receptor protein with no detectable B1 receptor protein. We conclude that BK evokes iCGRP release from bovine dental pulp which is enhanced by a positive interaction with PGE2. Neurosecretion is evoked from isolated terminals of dental pulp fibers via the bradykinin B2 receptor-dependent mechanism.

Analysis of Variance↗
PubMed1991

Neuropeptide Y potentiates luteinizing hormone (LH)-releasing hormone-stimulated LH surges in pentobarbital-blocked proestrous rats.

Recent evidence suggests that hypothalamic neurosecretion of neuropeptide Y (NPY) may be required for the preovulatory LH surge in female rats. Results of immunoneutralization and portal blood collection studies have suggested that NPY may serve to enhance the response of gonadotropes to the stimulatory action of LHRH. To directly test this hypothesis, the effects of NPY on LHRH-stimulated LH secretion were assessed in proestrous rats that were anesthetized with pentobarbital (PB) to block endogenous LHRH neurosecretion. Female rats were fitted with atrial catheters on diestrus. On proestrus, hourly blood samples were collected from 0900-2100 h. At 1330 h, rats received PB (40 mg/kg BW) or saline. Every 30 min from 1400-1800 h, PB-treated rats received iv pulses of LHRH (15, 150, or 1500 ng/pulse) or saline along with concurrent pulses of NPY (1 or 10 micrograms/pulse). Plasma samples were analyzed by LH RIA. In PB-treated rats receiving vehicle pulses only, LH surges were completely blocked. Pulsatile LHRH treatments at 15, 150, and 1500 ng/pulse produced subphysiological, physiological, and supraphysiological LH surges, respectively. Simultaneous administration of NPY pulses with 15 ng/pulse LHRH produced significant dose-related potentiations of LHRH-stimulated LH surges (P less than 0.0001). Administration of NPY pulses with 150 ng LHRH/pulse also significantly enhanced LHRH-induced LH surges (P less than 0.05). NPY RIA of plasma confirmed NPY increments after treatments. These results demonstrate that NPY administration can potentiate pituitary responsiveness to LHRH stimulation, and are consistent with the hypothesis that one function of NPY is to operate as a neurohormonal modulator at the level of the gonadotrope during generation of the preovulatory LH surge.

Animals↗
PubMed2000

Hrs interacts with SNAP-25 and regulates Ca(2+)-dependent exocytosis.

Synaptosome-associated protein of 25 kDa (SNAP-25) is a neuronal membrane protein essential for synaptic vesicle exocytosis. To investigate the mechanisms by which SNAP-25 mediates neurosecretion, we performed a search for proteins that interact with SNAP-25 using a yeast two-hybrid screen. Here, we report the isolation and characterization of a SNAP-25-interacting protein that is the rat homologue of mouse hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs). Hrs specifically interacts with SNAP-25, but not SNAP-23/syndet. The association of Hrs and SNAP-25 is mediated via coiled-coil interactions. Using an Hrs-specific antibody, we have shown that Hrs is highly enriched in brain, where it codistributes with SNAP-25 in most brain regions. Subcellular fractionation studies demonstrate that in brain, Hrs exists in both cytosolic and membrane-associated pools. Studies using indirect immunofluorescence and confocal microscopy reveal that, in addition to early endosomes, Hrs is also localized to large dense-core secretory granules and synaptic-like microvesicles in nerve growth factor-differentiated PC12 cells. Moreover, overexpression of Hrs in PC12 cells inhibits Ca(2+)-dependent exocytosis. These results suggest that Hrs is involved in regulation of neurosecretion through interaction with SNAP-25.

Amino Acid Sequence↗
PubMedDate not supplied

Effects of reducing agents on glutathione metabolism and the function of carotid body chemoreceptor cells.

Two current hypotheses of O2 sensing in the carotid body (CB) chemoreceptors suggest participation of oxygen reactive (ROS) species, but they are mechanistically opposed. One postulates that hypoxia decreases ROS levels; the other that hypoxia increases them. Yet, both propose that the ensuing alteration in the cellular redox environment is the key signal triggering hypoxic chemoreception. Since the glutathione redox pair is the main cellular buffer for ROS and the main determinant of the general redox environment of the cells, a way to test whether ROS participate in chemoreception is to determine glutathione levels and to correlate them with the activity of CB chemoreceptor cells. We found that hypoxia does not alter the glutathione reduction potential but that it activates chemoreceptor cell neurosecretion. Incubation of tissues with reduced glutathione increases the glutathione-reducing potential but does not activate chemoreceptor cells in normoxia nor does it modify hypoxic activation. Like reduced glutathione, N-acetylcysteine promoted a general reducing environment in the cells without alteration of chemoreceptor cell activity. N-(mercaptopropionyl)-glycine, like the two previous agents, increases the reduction potential of glutathione. In contrast, the compound activated chemoreceptor cells in normoxia, promoting a dose- and Ca(2+)-dependent neurosecretion and a potentiation of the hypoxic responses. The existence of multiple relationships between glutathione reduction potential in the cells and their activity indicates that the general cellular redox environment is not a factor determining chemoreceptor cell activation. It cannot be excluded that the local redox environments of restricted microdomain(s) in the cells with specific regulating mechanisms are important signals for chemoreceptor cell activity.

Animals↗
PubMed1977

Concept of paraneurons.

Paraneurons are those cells which have not been designated as neurons but are recognized as closely related to neurons on the basis of their fine structure (possession of neurosecretion-like and synaptic vesicle-like granules/vacuoles), metabolism (production of neurosecretion- and neurotransmitter-like substances) and origin (evidenced or proposed neuroectodermal). Some paraneurons are mainly endocrine in function, while others are sensory. Some should be called interneurons. There are graduations between these types of paraneurons; also a definite boundary between neurons and paraneurons can not be determined. Different types of paraneurons (together with some related neurons) are shown in Figure 1. Comments and discussions were given on the neuron-like characteristics of the individual paraneurons.

APUD Cells↗
PubMed2000

Muscarinic stimulation of alpha1E Ca channels is selectively blocked by the effector antagonist function of RGS2 and phospholipase C-beta1.

Neuronal alpha1E Ca channel subunits are widely expressed in mammalian brain, where they are thought to form R-type Ca channels. Recent studies have demonstrated that R-type channels contribute to neurosecretion and dendritic Ca influx, but little is known concerning their modulation. Here we show that alpha1E channels are strongly stimulated, and only weakly inhibited, through M1 muscarinic acetylcholine receptors. Both forms of channel modulation are mediated by pertussis toxin-insensitive G-proteins. Channel stimulation is blocked by regulator of G-protein signaling 2 (RGS2) or the C-terminal region of phospholipase C-beta1 (PLCbeta1ct), which have been previously shown to function as GTPase-activating proteins for Galphaq. In contrast, RGS2 and PLCbeta1ct do not block inhibition of alpha1E through M1 receptors. Inhibition is prevented, however, by the C-terminal region of beta-adrenergic receptor kinase 1, which sequesters Gbetagamma dimers. Thus, stimulation of alpha1E is mediated by a pertussis toxin-insensitive Galpha subunit (e.g., Galphaq), whereas inhibition is mediated by Gbetagamma. The ability of RGS2 and PLCbeta1ct to selectively block stimulation indicates these proteins functioned primarily as effector antagonists. In support of this interpretation, RGS2 prevented stimulation of alpha1E with non-hydrolyzable guanosine 5'-0-(3-thiotriphosphate). We also report strong muscarinic stimulation of rbE-II, a variant alpha1E Ca channel that is insensitive to voltage-dependent inhibition. Our results predict that Galphaq-coupled receptors predominantly stimulate native R-type Ca channels. Receptor-mediated enhancement of R-type Ca currents may have important consequences for neurosecretion, dendritic excitability, gene expression, or other neuronal functions.

Animals↗
PubMed1975

[Trigger properties of gonadotropic hormones and oocyte factors in connection with the germinal epithelium of the rat testis].

In order to reveal possible stimulation of growth of the germinal epithelium of the rat's injured testicle the animals were injected follicle-stimulating and luteinizing hormones and their mixture as well as homogenate of fertilized egg-cells during two weeks. Changes of neurosecretion in large-cell nuclei of the anterior hypothalamus, cellular set in the adenohypophysis and the condition of the germinal epithelium in the gonad under study were investigated. Identical phenomena of reduction (having quantitative distinctions) took place due to effects of exogeneous honadotropins in neurosecretory nuclei and the adenohypophysis. In testicular tubules there occurred pronounced proliferation of the germinal epithelium, but spermatogenesis was absent. Egg-cell homogenate failed to cause changes in neurosecretion and adenohypophysis but resulted in completing the developmental cycle of the germinal epithelium with mature spermatozoa. The effect of gonadotropins upon the system hypothalamus-hypophysis is explained by feed-back mechanism, and the absence of spermatogenesis--by the lack of androgens. The rsults of egg-cell homogenate effects should be associated with local stimulating effects of DNA of the dividing egg-cell.

Animals↗
PubMed1992

Neuropeptide Y: a novel neuroendocrine peptide in the control of pituitary hormone secretion, and its relation to luteinizing hormone.

Evidence that establishes neuropeptide Y (NPY) as an important neuromessenger in the regulation of anterior pituitary hormone secretion is reviewed. In particular, NPY plays a critical role in stimulating the episodic, basal pattern of luteinizing hormone (LH) release, as well as the preovulatory surge of LH release in several species. The stimulatory effect of NPY on LH secretion is dependent upon the presence of gonadal hormones and involves amplification of the response of other interacting stimulatory signals. NPY acts at the level of the median eminence to excite the release of LH-releasing hormone (LHRH) via a mechanism that leads to the mobilization of intracellular Ca2+. These stimulatory LHRH responses are mediated by Y1NPY receptors. Moreover, NPY activates postsynaptic messenger pathways that complement and reinforce those affected by norepinephrine, which is another major neuroregulator of LHRH secretion and which is released as a cotransmitter with NPY in the median eminence. Additionally, NPY is released into the hypophyseal portal blood for transportation to the anterior pituitary where it enhances the release of LH in response to LHRH. This facilitatory, modulating effect at the pituitary level involves an allosteric increase in LHRH binding to its receptor leading to augmented influx of Ca2+ from the extracellular space. There is evidence that gonadal steroids regulate NPY neurosecretion in a site-specific manner, and that alterations in NPY secretion may occur in part via a direct action of the steroids on NPY neurons in the brainstem and hypothalamus and in part through an indirect effect involving removal of the inhibitory influence of endogenous opioid peptides. These findings are integrated into an overall hypothesis for induction of the preovulatory LH surge on proestrus requiring an interplay between NPY and other neuronal networks. In aged male rats, due to the inability of hypothalamic NPY neurons to respond appropriately to the trophic effects of androgens, NPY neurosecretion is diminished. Further, a review of the literature reveals that NPY may modulate the secretion of other pituitary hormones through a similar combination of hypothalamic and pituitary actions.

Amino Acid Sequence↗
PubMed1990

[The effect of vitamin E on the neurosecretory cells of the hypothalamus in white rats].

For analysing the earlier detected hormone-depending effect of vitamin E (alpha-TPh) on functional systems of the organism, a study was made of the influence of this vitamin on the morphometric indexes of functional conditions of supraoptic (SON), suprachiasmatic (SCN), paraventricular (NPV) and arcuate (AN) hypothalamic centres. Experiments were performed on Wistar rats (males and females) either of which was given per os a 5 mg daily dose of 5% D, L, alpha-tocopherol-acetate oil solution for three weeks. In results, a repression of functional activity of the neurosecretion cells (decrease in nuclear dimensions) was shown. Such an influence was found in all the centres studied except the SON which, on the contrary, was seen stimulated. Besides, considerable changes in nuclear and nucleolar dimensions were seen on histograms estimated by criterion lambda according to Kholmogorov and Smirnov. The results obtained can be possibly explained by differences in the initial levels of endogenic alpha-TPh and of other antioxidants in the cell membrane matrix of the hypothalamic centres, and, correspondingly, by different modulation effects of alpha-TPh exerted on the functional condition of neurosecretion cells.

Animals↗
PubMed1975

[Reaction of the neurosecretory system of dogs with reno-vascular hypertension in the postnatal ontogenesis].

In dogs of different age with simulated renovascular hypertension neurosecretion of the hypothalamo-neurohypophysial system was studied. Experiments were conducted with puppies 18-22 days, 11/2-3 months and dogs 3-5 years old. It was established that in the ontogenesis of dogs the differentiation of neurons in the supraoptic nucleus occurred earlier than that of cells in the paraventricular nucleus. The simulation of hypertension accelerates the differentiation of tbe neurosecretory cells. The development of arterial hypertension leads to prevalence of precesses of the neurosecretory material outflow over the latter's synthesis, irrespective of the maturity of the neurosecretory system. With the arterial pressure stabilized at a high level a concordance between an elevated synthesis of the neurosecretion and its increased outflow is noted. Visual evaluation of the activity is supported by the results of cellular micrometry.

Age Factors↗
PubMed1989

A role for cGMP during tetanus toxin blockade of acetylcholine release in the rat pheochromocytoma (PC12) cell line.

In order to identify the specific molecular mechanisms involved in neurosecretion, we investigated the mechanism of action of tetanus toxin, a potent presynaptic neurotoxin, in the rat adrenal pheochromocytoma PC12 cell line. It has recently been reported that tetanus toxin is a potent inhibitor of the release of depolarization-evoked 3H-acetylcholine (ACh) from nerve growth factor-differentiated PC12 cells (Sandberg et al., 1989a). In PC12 cells, as in many neural tissue preparations, cGMP accumulation in intact cells increased 6- to 17-fold when stimulated with veratridine (200 microM), carbachol (1 mM), Ba2+ (2 mM), or K+ (30 mM). Preincubation of the cells with tetanus toxin inhibits this accumulation by greater than 95%. The toxin dose-inhibition curves for 3H-ACh release and cGMP accumulation are similar, with half-maximal doses of tetanus toxin seen at approximately 5 nM. The time courses for the development of the effects of tetanus on 3H-ACh release and on cGMP accumulation were also similar. Protocols which elevated intracellular cGMP levels reversed the action of the toxin. For example, evoked ACh release was restored in intoxicated PC12 cells by a 15 min exposure to 100 microM 8-bromo-cGMP. The half-maximal dose was observed at 50 microM nucleotide. Examination of the nucleotide specificity revealed that only cyclic guanine analogs were effective in reversing the effects of tetanus toxin. These results suggested that the inhibition of depolarization-evoked cGMP accumulation is causally related to the action of tetanus toxin on neurosecretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1985

[Rhythmicity of the activity of the supraoptic and paraventricular nuclei of the hypothalamus of the C57Bl mouse].

Rhythmical changes in the activity of the neurosecretory processes have been compared in the supraoptic (SON) and paraventricular (PVN) nuclei in the C57Bl mice hypothalamus during vernal equinox. Parts of the neurosecretory cells, being at stages of synthesis, excretion and accumulation of secrete, volumes of the cell nuclei and nucleoli survey as criteria of their activity. Similar feature for the rhythmic of both nuclei studied is the highest activation of the processes during day time, when mice are resting; this is demonstrated as the maximal amount of actively synthesizing cells, maximal volumes of the cell nuclei and nucleoli. The peculiarities of the rhythmic display in the activity is manifested as a greater ability of the SON cells to accumulate neurosecrete. The accumulation of the secretory material in the SON cells precedes to the period of its maximal activity (1-7 PM) characterized: by making the cells free from the secrete and by a maximal increasing the volume of the nucleoli. In the PVN intensified display of the activity is noted at early hours of the day, and the amount of the cells not containing the secrete--at 6 PM. Lack of the neurosecrete accumulation in the PVN cells speaks in favour of more steady than in the SON cells excretion of the secrete. This demonstrates a more even maintenance of neurohormones concentration in the organism.

Animals↗
PubMed1984

[In vitro culture of the hypothalamic supraoptic nucleus. I. General morphological characteristics].

Kinetics and morphology of supraoptic nuclei (SON) organ culture of newborn rat hypothalamus have been described. Explants of SON were cultured for 7-90 days. Cell migration, growth of neuron sprouts, formation of nerve bundles and growth zone, and mitotic activity were followed. Neurosecretory cells (NSC) differing in size, shape and degree of activity, were identified in addition to other cell elements of SON. The neurosecret was shown to appear at the beginning of the second week of cultivation in large and middle size NSC. In small and old cultures of NSC no neurosecrete was discovered. It was established that NSC complete the terminal differentiation and maintain for a long time their viable and functional activity in vitro.

Animals↗
PubMed1983

[Host-parasite relations of the trematode Microphallus papillorobustus (Rankin, 1940). II-Changes in the behavior of Gammarus intermediate hosts and localization of metacercaria].

The aberrant behaviour observed in some Gammarids is correlated with the presence, in their brain, of mature metacercriae of Microphallus papillorobustus. Young cerebral larvae and mature thoracic or abdominal cysts of this Trematode do not induce alterations of behaviour in their hosts. Gammarus insensibilis and Gammarus aequicauda show different patterns in the distribution of M. papillorobustus larvae. Whereas many metacercariae are found in the thorax or abdomen of G. aequicauda adult, very few are present in this same location in G. insensibilis. Field data and experimental infections show that the post-cercariae encyst in the cerebroid ganglions in juveniles of both species as well as in adults of G. insensibilis; the post-cercariae encyst in the thorax or in the abdomen in adult G. aequicauda. The larvae could be attracted to the Amphipods' brain by a neurosecretion characteristic of young stages; this neurosecretion would still be produced at a high rate in adult G. insensibilis.

Animals↗