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dc.contributor.authorRyan, Jennifer Susan.en_US
dc.date.accessioned2014-10-21T12:33:55Z
dc.date.available1999
dc.date.issued1999en_US
dc.identifier.otherAAINQ49289en_US
dc.identifier.urihttp://hdl.handle.net/10222/55671
dc.descriptionThe pigmented cells of the retinal pigment epithelium (RPE) and the ciliary body epithelium (CBE) of the vertebrate eye are both transporting epithelia. The pigmented (PCE) cells of the CBE, together with the nonpigmented epithelial cells, are responsible for the secretion of aqueous humor into the posterior chamber. In this study, receptor and G-protein-coupled signaling pathways regulating ion channels in cultured RPE and PCE cells were examined.en_US
dc.descriptionUnder control conditions, a TEA and 4-AP-sensitive delayed outwardly rectifying K+ current (IK), a Ba2+-sensitive inwardly rectifying K+ current (IKi), and an inactivating outward K+ current were recorded in rat RPE cells. A large non-inactivating, nonselective cation (NSC) channel activated by non-hydrolyzable G protein analogues (GTPgammaS or Gpp(NH)p), was also identified in rat RPE cells. Blocking G proteins of the Gi/o/t/z class with pertussis toxin (PTX) or with antibodies against Galphai subunits abolished current activation, confirming involvement of a Galphai subunit protein.en_US
dc.descriptionIn rat RPE cells, application of ATP activated a cation conductance via actions on purine receptors. The electrophysiological characteristics of this current suggests that ATP activates P2X purinoceptors in rat RPE. In many cell types, ATP can also act on metabotropic P2Y pruinoceptors coupled to a phospholipase C (PLC)/inositol triphosphate (IP3) signaling pathway and intracellular Ca2+ stores release. In 38% of rat RPE cells recorded from, ATP also activated an iberiotoxin (IbTX)-sensitive Ca2+-activated K+ current (IK(Ca)).en_US
dc.descriptionIn cultured rabbit PCE cells, inwardly and outwardly rectifying K + conductances were recorded. A portion of the outward K+ current was dependent on Ca2+ and was sensitive to IbTX, demonstrating the presence of K(Ca) channels. The adrenergic agonists epinephrine (EPI) and phenylephrine (PHe) increased IK(Ca). PHe-mediated increases in IK(ca) activity were blocked by the adrenergic antagonist, prazosin, confirming the involvement of alpha-adrenoceptors. (Abstract shortened by UMI.)en_US
dc.descriptionThesis (Ph.D.)--Dalhousie University (Canada), 1999.en_US
dc.languageengen_US
dc.publisherDalhousie Universityen_US
dc.publisheren_US
dc.subjectHealth Sciences, Pharmacology.en_US
dc.titleMolecular signaling pathways regulating cation channels in ocular epithelial cells.en_US
dc.typetexten_US
dc.contributor.degreePh.D.en_US
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