Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neurosecretion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1994

NEUROSECRETION OF CRUSTACEAN HYPERGLYCEMIC HORMONE EVOKED BY AXONAL STIMULATION OR ELEVATION OF SALINE K+ CONCENTRATION QUANTIFIED BY A SENSITIVE IMMUNOASSAY METHOD

A sandwich-type enzyme-linked immunosorbent assay (ELISA) was utilized to quantify crustacean hyperglycemic hormone (as Carcinus maenas equivalents) released by single X-organ­sinus gland systems of the crab Cardisoma carnifex during continuous perifusion. Basal rates of secretion (20­60 pg min-1) were stable for at least 4 h. Electrical stimulation (600 stimuli in 5 min) of the axon tract increased secretion two- to threefold, but only if it resulted in neural activity that was propagated to the terminals of the sinus gland. No difference was observable when stimuli were given repetitively or as a series of trains. Perifusion with saline having ten times the normal K+ concentration augmented secretion by as much as fivefold. Augmented secretion of crustacean hyperglycemic hormone evoked by either electrical or K+ stimulation appeared abruptly but declined slowly (over tens of minutes) after stimulation was stopped. K+-evoked secretion of crustacean hyperglycemic hormone was maintained without decrement for at least 1 h. Basal secretion increased in saline from which Ca2+ had been omitted, but decreased in saline containing Mn2+. Neither electrical stimulation nor high [K+] augmented secretion in Ca2+-deficient saline or if Mn2+ was present. Introduction of Mn2+ during K+-evoked secretion immediately reduced release to unstimulated levels; secretion resumed promptly upon removal of Mn2+. Tetrodotoxin reversibly blocked both electrical and secretory responses to axonal stimulation, but it did not block basal or K+-evoked secretion. Release of crustacean hyperglycemic hormone by isolated axon terminals was augmented two- to threefold by perifusion with saline having ten times the normal K+ concentration. The responses were similar to those of the intact systems, having a rapid onset, well-maintained secretion and a long 'tail' of secretion after removal of the K+ stimulus.

Journal Article↗
PubMed1977

The role of neurosecretion in the photoperiodic control of polymorphism in the aphid Megoura viciae.

The location of the photoperiodic mechanism controlling the production of the sexual and parthenogenetic morphs by apterous parents was examined by selectively injuring the brain with an R.F. microcautery. Lesions destroying the Group I neurosecretory cells (NSC) in the protocerebrum abolished the response to changed daylength. Extensive damage to other NSC Groups, to the compound eyes and optic lobes was without effect. It is concluded that the Group I NSC are the effectors, secreting a virginoparapromoting substance; in its absence only oviparae are produced. Areas slightly lateral to the group I NSC are also required for the long-day response, indicating that this is the probable site of the neuronal photoperiodic clock which regulates the release of neurosecretory material (NSM) from the Group I cells.

Animals↗
PubMed2005

Using microarrays to facilitate positional cloning: identification of tomosyn as an inhibitor of neurosecretion.

Forward genetic screens have been used as a powerful strategy to dissect complex biological pathways in many model systems. A significant limitation of this approach has been the time-consuming and costly process of positional cloning and molecular characterization of the mutations isolated in these screens. Here, the authors describe a strategy using microarray hybridizations to facilitate positional cloning. This method relies on the fact that premature stop codons (i.e., nonsense mutations) constitute a frequent class of mutations isolated in screens and that nonsense mutant messenger RNAs are efficiently degraded by the conserved nonsense-mediated decay pathway. They validate this strategy by identifying two previously uncharacterized mutations: (1) tom-1, a mutation found in a forward genetic screen for enhanced acetylcholine secretion in Caenorhabditis elegans, and (2) an apparently spontaneous mutation in the hif-1 transcription factor gene. They further demonstrate the broad applicability of this strategy using other known mutants in C. elegans,Arabidopsis, and mouse. Characterization of tom-1 mutants suggests that TOM-1, the C. elegans ortholog of mammalian tomosyn, functions as an endogenous inhibitor of neurotransmitter secretion. These results also suggest that microarray hybridizations have the potential to significantly reduce the time and effort required for positional cloning.

Journal Article↗
PubMed2006

Centrally administered neuropeptide W-30 activates magnocellular neurosecretory cells in the supraoptic and paraventricular nuclei with neurosecretion in rats.

We examined the effects of i.c.v. administration of neuro-peptide W-30 (NPW30) on plasma arginine vasopressin (AVP) and plasma oxytocin (OXT) using RIA. The induction of c-fos mRNA, AVP heteronuclear (hn)RNA, and c-Fos protein (Fos) in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of rats were also investigated using in situ hybridization histochemistry for c-fos mRNA and AVP hnRNA, and immunohistochemistry for Fos. Both plasma AVP and OXT were significantly increased at 5 and 15 min after i.c.v. administration of NPW30 (2.8 nmol/rat). In situ hybridization histochemistry revealed that the induction of c-fos mRNA and AVP hnRNA in the SON and PVN were significantly increased 15, 30, and 60 min after i.c.v. administration of NPW30 (1.4 nmol/rat). Dual immunostaining for Fos/AVP and Fos/OXT revealed that both AVP-like immunoreactive (LI) cells and OXT-LI cells exhibited nuclear Fos-LI in the SON and PVN, 90 min after i.c.v. administration of NPW30 (2.8 nmol/rat). These results suggest that central NPW30 may be involved in the regulation of secretion of AVP and OXT in the magnocellular neurosecretory cells in the SON and PVN.

Animals↗
PubMedDate not supplied

[alpha-Latrotoxin as an instrument for studying neurosecretions].

alpha-Latrotoxin, a presynaptic toxin from black widow spider venom Latrodectus mactans tredecimguttatus, triggers exocytosis in a variety of neurosecretory cells both in the presence and absence of calcium in the medium. The toxin interacts with two types of membrane the receptors which belong to different families of neuronal proteins and have different structures. Calcium-dependent receptor of alpha-latrotoxin is identified as neurexin I alpha and belongs to the family of neurexins. This family is selectively expressed in nerve tissue. The calcium-independent receptor of alpha-latrotoxin belongs to the family of G-protein-coupled receptors and proteins which homologous to it are found in heart, lung, kidney and spleen tissues. As a result of alpha-latrotoxin interaction with membrane receptor in the calcium medium the toxin forms the ionic channels in plasmalemma and enhances its calcium permeability. The effects of alpha-latrotoxin on exocytosis in the calcium and calcium-free media and question concerning coupling of channel-forming and secretogenic properties of alpha-latrotoxin are discussed.

Exocytosis↗
PubMed2001

[Presynaptic 5-hydroxytryptamine receptors enhance cholinergic neurosecretion in the human iris-ciliary body].

OBJECTIVE: To characterize presynaptic 5-hydroxytryptamine (5-HT) heteroreceptors which modulate 3H-acetylcholine (3H-ACh) release in isolated human iris-ciliary bodies (ICBs). METHODS: ICB tissue segments were perfused and incubated with 3H-choline, and electrically stimulated four times (S1, S2, S3 and S4) at 10 Hz for 1 min to elicit 3H-ACh secretion. Test agents, 5-HT agonists and antagonists, were added before S2, S3 and S4 and their effects were determined by the stimulation ratio (Sx/S1) of evoked 3H-ACh release. 3H-ACh in perfusate fractions was isolated by ion exchange chromatography and analyzed for radioactivity by liquid scintillation spectrometry. RESULTS: The evoked 3H-ACh release was enhanced in a concentration-dependent manner by 5-HT [10(-9)-10(-5) mol/L, 50% effective concentration values (EC50) = 3.36 x 10(-8) mol/L] as well as 5-methoaxytryptamine [5-MOT (agonist), 10(-8)-10(-5) mol/L, EC50 = 6.59 x 10(-7) mol/L]. The selective 5-HT4 antagonist, GR113808A (10(-8) mol/L) inhibited the 5-HT-inducing increase of the cholinergic response, producing parallel right shifts of the 5-HT concentration-response curves (t = 4.012, P < 0.01). The selective 5-HT3 antagonist ondersetron (5 x 10(-7) mol/L) and tropisetron (10(-9) mol/L) did not affect 5-HT inducing 3H-Ach release (t = 2.215, P > 0.05). CONCLUSION: Our results indicate that cholinergic terminals in the human ICB contain 5-HT heteroreceptors that may promote the release of 5-HT and belong to the 5-HT4 subtype.

5-Methoxytryptamine↗
PubMed2003

Regulation of cyclic adenosine 3',5'- monophosphate signaling and pulsatile neurosecretion by Gi-coupled plasma membrane estrogen receptors in immortalized gonadotrophin-releasing hormone neurons.

Immortalized GnRH neurons (GT1-7) express receptors for estrogen [estrogen receptor-alpha and-13(ERa and ERI3)] and progesterone (progesterone receptor A) and exhibit positive immunostaining for both intracellular and plasma membrane ERs. Exposure of GT1-7 cells to picomolar estradiol concentrations for 5-60 min caused rapid, sustained,and dose-dependent inhibition of cAMP production. In contrast, treatment with nanomolar estradiol concentrations for 60 min increased cAMP production. The inhibitory and stimulatory actions of estradiol on cAMP formation were abolished by the ER antagonist, ICI 182,780. The estradiol-induced inhibition of cAMP production was prevented by treatment with pertussis toxin, consistent with coupling of the plasma membrane ER to an inhibitory G protein. Coimmunoprecipitation studies demonstrated an estradiol-regulated stimulatory interaction between ERa and G,3 that was prevented by the ER antagonist, ICI 182,780. Exposure of perifused GT1-7 cells and hypothalamic neurons to picomolar estradiol levels increased the GnRH peak interval, shortened peak duration, and increased peak amplitude. These findings indicate that occupancy of the plasma membrane-associated ERs expressed in GT1-7 neurons by physio-logical estradiol levels causes activation of a G, protein and modulates cAMP signaling and neuropeptide secretion.

Animals↗
PubMedDate not supplied

[Modulating effect of anticonvulsive agents on Ca2+ dependent membrane fusion in cell-free model of neurosecretion].

The effect of antiepileptic drug ethosuximide and sodium valproat on fusion of synaptic vesicles with synaptosomal plasma membranes was studied in cell-free system. It was shown that ethosuximide and sodium valproat increases the rate of Ca(2+)-dependent fusion reaction in vitro. We have found that convulsant drugs pentylenetetrazol and picrotoxin did not fuse membrane components of the model system. Ethosuximide- and sodium valproat-provoked fusion of synaptic vesicles and plasma membranes of synaptosomes were suppressed by convulsant drugs pentylenetetrazol and picrotoxin.

Animals↗
PubMed1990

[The influence of CCNU (lomustine) on the neurosecretion of hypothalamic nuclei and the neurohypophysis during early stages of extrauterine development of the rat].

The hypothalamo-neurohypophyseal neurosecretory system was investigated in 8-, 15- and 30-day-old rats subjected to three intragastric doses of CCNU - 12.5 mg/kg b. wt. each on the 3rd, 5th and 7th day after birth. Neurosecretory neurons in the hypothalamus were visualized in the paraffin sections by the immunoenzyme (PAP) technique using antibodies against neurophysin and by Gomori chrome-hematoxylin staining. Accumulation of neurophysin was observed in these cells after treatment with CCNU. Karyometric measurements showed an increase of the mean nuclear cross-section area in PVN neurons in 8-day-old rats exposed to CCNU. In four experimental rats disseminated intracerebral hemorrhagic foci were present. Plasma osmolality was far below the normal values on the 8th day, on the 15th day of life it shifted to hyperosmolality and returned to normal at the age of 30 days. Discussion of the results leads to the conclusion that the increase of the neurosecretory function observed in this experiment was secondary to vasogenic changes.

Animals↗