Disease relevance of Neurosecretion

• The present results suggest that prolonged hypoxia can induce formation of Ca(2+)-permeable AbetaP channels and that such induction can lead directly to excessive neurosecretion [1].
• Effects of diltiazem (a calcium antagonist) on neurosecretion and vascular responsiveness in hypertension [2].
• The response of the HPNS was found to depend directly on the dose of lithium given and to consist of activation of synthesis and liberation of neurosecretion after a single dose of LiCl or inhibition of hormone formation in the hypothalamus and exhaustion of the reserves of neurosecretion in the neurohypophysis after a course of injections [3].
• The modification of experimental febrile convulsions by PACAP (pituitary adenylate cyclase-activating peptide) was investigated; PACAP is a physiological regulator of the neurosecretion of arginine-vasopressin [4].

Psychiatry related information on Neurosecretion

• 5. The neurosecretion evoked by tacrine could explain the therapeutic effects of the drug claimed in the treatment of Alzheimer's type of dementia [5].
• Episodic NPY neurosecretion in hypothalamic target sites is temporally linked with onset of the daily feeding pattern [6].

High impact information on Neurosecretion

• MARCKS is a specific protein kinase C (PKC) substrate that binds both calmodulin and actin and is phosphorylated during phagocyte activation, neurosecretion, and growth factor-dependent mitogenesis [7].
• Here we show that CFTR is regulated by an epithelially expressed syntaxin (syntaxin 1A), a membrane protein that also modulates neurosecretion and calcium-channel gating in brain [8].
• This mode of transmitter action may explain the ability of noradrenaline and GABA to presynaptically inhibit Ca2+-dependent neurosecretion from DRG sensory neurones [9].
• Sulfonylurea-sensitive adenosine triphosphate (ATP)-regulated potassium (KATP) channels are present in brain cells and play a role in neurosecretion at nerve terminals [10].
• These findings suggest that hypothalamic growth hormone-releasing factor may regulate its own neurosecretion through an "ultrashort-loop" negative feedback mechanism and may have important neurotransmitter and neuromodulatory functions in the brain [11].

Chemical compound and disease context of Neurosecretion

• We found that hypoxia does not alter the glutathione reduction potential but that it activates chemoreceptor cell neurosecretion [12].
• Role of substance P and neurotensin in the regulation of neurosecretion and vascular responsiveness in hypertension [13].

Biological context of Neurosecretion

• In the context of sensitized C nociceptors and in the absence of sympathetic vasoconstrictor deficit, the abnormally elevated temperature in symptomatic skin is interpreted as due to antidromic vasodilatation triggered by neurosecretion from hyperactive nociceptors.(ABSTRACT TRUNCATED AT 400 WORDS)[14]
• Here, we identify point mutants in Caenorhabditis elegans that map to highly conserved regions of the VAChT gene of Caenorhabditis elegans (CeVAChT) (unc-17) and exhibit behavioral phenotypes consistent with a reduction in vesicular transport activity and neurosecretion [15].
• When cells are treated with the protein synthesis inhibitor puromycin, after alkylation, receptor-mediated neurosecretion does not recover [16].
• These results suggest that RGS proteins may play important roles in shaping the magnitude and kinetics of physiological events, such as neurosecretion, that involve G protein-modulated Ca channels [17].
• Using digital imaging videomicroscopy to measure fluorescence resonance energy transfer in live neurons, we also found that taipoxin modulates the machinery for neurosecretion by causing dissociation of the SV proteins synaptobrevin 2 and synaptophysin I at a stage preceding taipoxin-induced facilitation of SV fusion [18].

Anatomical context of Neurosecretion

• These results indicate that SNIP is involved in regulation of neurosecretion, perhaps via its interaction with SNAP-25 and the cytoskeleton [19].
• Regulation of cyclic adenosine 3',5'-monophosphate signaling and pulsatile neurosecretion by Gi-coupled plasma membrane estrogen receptors in immortalized gonadotropin-releasing hormone neurons [20].
• SV2 (Synaptic Vesicle Protein 2) is expressed in neurons and endocrine cells where it is required for normal calcium-evoked neurosecretion [21].
• Nitric oxide implication in the control of neurosecretion by chromaffin cells [22].
• Somatostatin (SRIF) is a putative peptide neurotransmitter that may interact with brain capillaries following neurosecretion of the peptide [23].

Associations of Neurosecretion with chemical compounds

• Vasopressin and oxytocin in other hypothalamic nuclei may be a part of this system of neurosecretion or may serve some other function [24].
• Dependence of intracellular signaling and neurosecretion on phospholipase D activation in immortalized gonadotropin-releasing hormone neurons [25].
• Serotonin (5-HT) receptor subtypes mediate specific modes of 5-HT-induced signaling and regulation of neurosecretion in gonadotropin-releasing hormone neurons [26].
• The mechanisms of neurosecretion were evaluated further by inhibition of vesicular release with the use of Ca(2+)-free, Mg(2+)-enriched dialysis fluid and by local perfusion with inhibitors of voltage-dependent synaptic release (1 microM tetrodotoxin) and of GABA reuptake (0.5 mM nipecotic acid) [27].
• Bath application of dopamine reduced the quantal content at single release sites with a similar time course and concentration dependence as that observed for the e.j.p. Dopamine had no effect on histograms of synaptic delays determined over a 10 degree C range, indicating that it does not modify the time course of phasic neurosecretion [28].

Gene context of Neurosecretion

• These results suggest that Hrs is involved in regulation of neurosecretion through interaction with SNAP-25 [29].
• 7. Thus Q-channels are present on a subset of the neurohypophysial terminals where, in combination with N- and L-channels, they control AVP but not OT peptide neurosecretion [30].
• 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 [31].
• In vertebrates, the appropriate neurosecretion of the decapeptide gonadotropin-releasing hormone (GnRH) plays a critical role in the progression of puberty [32].
• Interaction of CIRL with a specific presynaptic neurotoxin and with a component of the docking-fusion machinery suggests its role in regulation of neurosecretion [33].

References