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Purinergic receptor activation evokes neurotrophic factor NPY release from mouse olfactory epithelial slices
Author(s) -
Hegg Colleen Cosgrove,
Kanekar Shami
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1314-a
Subject(s) - ppads , purinergic receptor , neurotrophic factors , endocrinology , medicine , olfactory epithelium , p2 receptor , receptor , suramin , neurotrophin , biology , purinergic signalling , p2y receptor , brain derived neurotrophic factor , microbiology and biotechnology , chemistry , adenosine receptor , agonist
The signals for injury‐evoked neuroregeneration are unknown; however previous studies implied that injured cells secrete neurotrophic factors which trigger neurogenesis. Extracellular purine nucleotides exert multiple neurotrophic actions in the CNS mediated via activation of purinergic (P2) receptors. Our previous work demonstrated that ATP acts as a neuromodulator and a stress signal in the olfactory epithelium (OE). To determine whether ATP and P2 receptor activation evokes neurotrophic factor secretion in the OE, we monitored release of NPY, a neuroproliferative factor known to be present and functional in the OE. Neonatal mouse OE slices were cultured on nitrocellulose paper to visualize NPY release. Immunoassaying the nitrocellulose resulted in NPY immunoreactivity in the region corresponding to the OE of the nasal septum. Exogenous ATP (10–500 mM) significantly increased the percentage of OE slices that released NPY from 22% to 46% (p<0.05). P2 receptor antagonists PPADS (25 mM) and suramin (100 mM) reduced the number of OE slices exhibiting NPY release evoked by ATP by 53%, suggesting that activation of P2 receptors mediates NPY release. This study directly verifies that neurotrophic factor ATP evokes neurotrophic factor NPY release in the OE and provides pharmacological targets to promote regeneration of damaged OE. Research supported by NIH NIDCD DC006897.