neuropeptide-y and pyridoxal-phosphate-6-azophenyl-2--4--disulfonic-acid

neuropeptide-y has been researched along with pyridoxal-phosphate-6-azophenyl-2--4--disulfonic-acid* in 3 studies

Other Studies

3 other study(ies) available for neuropeptide-y and pyridoxal-phosphate-6-azophenyl-2--4--disulfonic-acid

ArticleYear
NPY mediates ATP-induced neuroproliferation in adult mouse olfactory epithelium.
    Neurobiology of disease, 2010, Volume: 38, Issue:3

    In the CNS, ATP is released upon injury and promotes neuroproliferation via purinergic receptors. In the olfactory epithelium, ATP promotes the synthesis and release of neurotrophic factor NPY in neonates and induces neuroproliferation in neonatal and adult mice. We tested the hypothesis that NPY is involved in ATP-induced neuroproliferation in adult mice olfactory epithelium. Intranasal instillation of ATP significantly increased protein levels and number of NPY(+) cells. Pre-intranasal instillation of purinergic receptor antagonist PPADS significantly reduced ATP-induced upregulation of NPY. Intranasal instillation of NPY-Y1 receptor antagonist BIBP3226 following ATP instillation significantly inhibited the ATP-induced increase in BrdU incorporation, suggesting that NPY is released after ATP instillation and activates Y1 receptors to promote neuroproliferation. These data indicate that ATP initiates neuroproliferation via NPY upregulation, NPY release, and Y1 receptor activation, and suggests that the olfactory epithelium is good model to study neuroregenerative mechanisms in the CNS.

    Topics: Adenosine Triphosphate; Aging; Animals; Arginine; Cell Proliferation; Dose-Response Relationship, Drug; Male; Mice; Models, Neurological; Neurogenesis; Neuropeptide Y; Olfactory Mucosa; Purinergic Antagonists; Pyridoxal Phosphate; Receptors, Neuropeptide Y; Receptors, Purinergic; Sensory Receptor Cells

2010
Purinergic receptor activation evokes neurotrophic factor neuropeptide Y release from neonatal mouse olfactory epithelial slices.
    Journal of neuroscience research, 2009, May-01, Volume: 87, Issue:6

    One premise regarding the mechanism of injury-evoked neuroregeneration is that injured cells induce the release of neurotrophic factors to trigger neurogenesis. Extracellular purine nucleotides exert multiple neurotrophic actions in the central nervous system mediated via activation of purinergic receptors. However, whether purinergics have a neurotrophic role in the olfactory neuroepithelium has not been investigated. Thus, we monitored the ATP-induced release of neuropeptide Y (NPY), a neuropeptide that increases neuroproliferation in the olfactory epithelium. To visualize NPY release, slices of olfactory epithelium from neonatal mice were cultured on nitrocellulose paper. Immunoassays of the nitrocellulose demonstrated NPY immunoreactivity in regions corresponding to the olfactory epithelium of the nasal cavity. One hour of exposure to exogenous ATP (100, 500 microM) significantly increased the number of olfactory epithelium slices that released NPY from 25% +/- 6% to 60% +/- 7% or 71% +/- 10% (P = 0.001). The purinergic receptor antagonists pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS; 25 microM) and suramin (100 microM) significantly reduced the number of olfactory epithelium slices exhibiting ATP-evoked NPY release to 18% +/- 11% (P = 0.004), indicating that NPY release is mediated by activation of purinergic receptors. Released NPY was quantified by enzyme and radioimmunoassays. Exogenous ATP or UTP significantly increased the amount of NPY released. Overall, this study demonstrates that purinergic receptor activation mediates the release of neurotrophic factor NPY in the olfactory epithelium and provides pharmacological targets to promote regeneration of damaged olfactory epithelium.

    Topics: Adenosine Triphosphate; Analysis of Variance; Animals; Animals, Newborn; Collodion; Immunoassay; Immunohistochemistry; In Vitro Techniques; Mice; Neuropeptide Y; Olfactory Mucosa; Purinergic Antagonists; Pyridoxal Phosphate; Receptors, Purinergic; Suramin; Uridine Triphosphate

2009
Mechanisms underlying spontaneous rhythmical contractions in irideal arterioles of the rat.
    The Journal of physiology, 1999, Dec-01, Volume: 521 Pt 2

    1. Mechanisms underlying spontaneous rhythmical contractions have been studied in irideal arterioles of the rat using video microscopy and electrophysiology. 2. Rhythmical contractions (4 min-1) were more common during the second and third postnatal weeks and were always preceded by large, slow depolarizations (5-40 mV). 3. Spontaneous contractions were unaffected by tetrodotoxin (1 microM), neurotransmitter receptor antagonists, the sympathetic neurone blocker, guanethidine (5 microM) or sensory neurotoxin, capsaicin (1 microM). 4. Stimulation of sensory nerves inhibited spontaneous activity and this was not prevented by L-NAME (10 microm). 5. L-NAME (10 microm) caused an increase in frequency of spontaneous contractions, while forskolin (30 nM), in the presence of L-NAME, abolished spontaneous, but not nerve-mediated, contractions. 6. Spontaneous activity was not affected by felodipine (1 nM) or nifedipine (1 microM), but was abolished by cadmium chloride (1 microM) or superfusion with calcium-free solution. 7. Caffeine (1 mM), thapsigargin (2 microM) and cyclopiazonic acid (3 microM), but not ryanodine (3 microM), abolished spontaneous and nerve-mediated contractions. After preincubation in L-NAME (10 microM), cyclopiazonic acid abolished spontaneous contractions only. 8. Spontaneous depolarizations and contractions were abolished by 18alpha-glycyrrhetinic acid (20 microM). 9. Results suggest that spontaneous rhythmical contractions are myogenic and result from the cyclical release of calcium from intracellular stores, without a contribution from voltage-dependent calcium channels. Intercellular coupling through gap junctions appears to be essential for co-ordination of these events which could be modulated by nitric oxide and increases in cAMP. The possibility that different intracellular stores underly spontaneous and nerve-mediated contractions is discussed.

    Topics: Adenosine Triphosphate; Age Factors; Animals; Arterioles; Cadmium Chloride; Caffeine; Calcium; Capsaicin; Central Nervous System Stimulants; Colforsin; Cyclic AMP; Dinucleoside Phosphates; Enzyme Inhibitors; Felodipine; Female; Gap Junctions; Iris; Male; Membrane Potentials; Muscle, Smooth, Vascular; Neuropeptide Y; NG-Nitroarginine Methyl Ester; Peptides, Cyclic; Periodicity; Platelet Aggregation Inhibitors; Pyridoxal Phosphate; Rats; Rats, Wistar; Ryanodine; Thapsigargin; Vasoconstriction; Vasodilator Agents

1999