Inhibitors of cAMP phosphodiestereses (PDEs) promoted an increase in intracellular [cAMP]c and an influx of Ca2+, in both MMQ pituitary cells and α-Pancreatic cells. The specific targets for PDEs and the domains of PDEs are still unknown. Pituitary MMQ cells were used as a model to test modulation of calcium influx through the L-type calcium channel with PDE inhibitors. cAMP analogs were used to determine cAMP molecular targets. 8-cpt-cAMP initiated an Epac mediated pathway and had strong effects on calcium influx in the cell; suggesting, a relatively strong cAMP target. Experiments of α-Pancreatic cells were done in 2mM glucose and 8mM glucose to stimulate hypoglycemia and resting states respectively. Ca2+ induced Ca2+ release (CICR) was observed when αMSH was applied with the three PDE inhibitors. When αMSH was applied without a PDE inhibitor there was no increase in [cAMP]c, suggesting a micro domain. Extracellular solutions of 2mM glucose with PDE inhibitors such as Milironone, there was influx through N-type and L-type channels and then steady CICR. Rolipram decreased the amount of [Ca2+]c influx compared to the control, suggesting an inhibitory effect. PDE locations within the cell dictate the level of [cAMP]c increase and the influx of [Ca2+]c.
","abstract_html":"<p>Inhibitors of cAMP phosphodiestereses (PDEs) promoted an increase in intracellular [cAMP]<sub>c</sub> and an influx of Ca<sup>2+</sup>, in both MMQ pituitary cells and α-Pancreatic cells. The specific targets for PDEs and the domains of PDEs are still unknown. Pituitary MMQ cells were used as a model to test modulation of calcium influx through the L-type calcium channel with PDE inhibitors. cAMP analogs were used to determine cAMP molecular targets. 8-cpt-cAMP initiated an Epac mediated pathway and had strong effects on calcium influx in the cell; suggesting, a relatively strong cAMP target. Experiments of α-Pancreatic cells were done in 2mM glucose and 8mM glucose to stimulate hypoglycemia and resting states respectively. Ca<sup>2+</sup> induced Ca<sup>2+</sup> release (CICR) was observed when αMSH was applied with the three PDE inhibitors. When αMSH was applied without a PDE inhibitor there was no increase in [cAMP]<sub>c</sub>, suggesting a micro domain. Extracellular solutions of 2mM glucose with PDE inhibitors such as Milironone, there was influx through N-type and L-type channels and then steady CICR. Rolipram decreased the amount of [Ca<sup><sub>2+</sub></sup>]<sub>c</sub> influx compared to the control, suggesting an inhibitory effect. PDE locations within the cell dictate the level of [cAMP]<sub>c</sub> increase and the influx of [Ca<sup>2+</sup>]<sub>c</sub>.</p>","abstract_has_math":false,"creators":["Crane, Colette"],"institution":null,"degree_name":"M.S.","degree_level":"Masters Thesis","degree_discipline":null,"degree_department":null,"school":null,"contributors":["Joseph K. Angleson, Ph.D.","Robert Dores","Nancy Lorenzon","Dwight Smith"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-06-01T07:00:00Z","date_published":"2011-06-01T07:00:00Z","updated_at":"2026-07-24T02:03:03Z","subjects":["Inhibitors of cAMP phosphodiestereses","Modulation of calcium influx","Endocrine cells","Biology","Life Sciences"],"languages":["en"],"rights":["Copyright is held by the author. User is responsible for all copyright compliance.
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"]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["cAMP and Calcium Interactions in Endocrine Cells"]}]}],"canonical_facts":{"dc:contributor":["Joseph K. Angleson, Ph.D.","Robert Dores","Nancy Lorenzon","Dwight Smith"],"dc:creator":["Crane, Colette"],"dc:date.available":["2001-01-01T08:00:00Z"],"dc:description.abstract":["Inhibitors of cAMP phosphodiestereses (PDEs) promoted an increase in intracellular [cAMP]c and an influx of Ca2+, in both MMQ pituitary cells and α-Pancreatic cells. The specific targets for PDEs and the domains of PDEs are still unknown. Pituitary MMQ cells were used as a model to test modulation of calcium influx through the L-type calcium channel with PDE inhibitors. cAMP analogs were used to determine cAMP molecular targets. 8-cpt-cAMP initiated an Epac mediated pathway and had strong effects on calcium influx in the cell; suggesting, a relatively strong cAMP target. Experiments of α-Pancreatic cells were done in 2mM glucose and 8mM glucose to stimulate hypoglycemia and resting states respectively. Ca2+ induced Ca2+ release (CICR) was observed when αMSH was applied with the three PDE inhibitors. When αMSH was applied without a PDE inhibitor there was no increase in [cAMP]c, suggesting a micro domain. Extracellular solutions of 2mM glucose with PDE inhibitors such as Milironone, there was influx through N-type and L-type channels and then steady CICR. Rolipram decreased the amount of [Ca2+]c influx compared to the control, suggesting an inhibitory effect. PDE locations within the cell dictate the level of [cAMP]c increase and the influx of [Ca2+]c.
"],"dc:format":["application/pdf"],"dc:identifier":["https://digitalcommons.du.edu/etd/145"],"dc:language":["en"],"dc:rights":["Copyright is held by the author. User is responsible for all copyright compliance.
"],"dc:subject":["Inhibitors of cAMP phosphodiestereses","Modulation of calcium influx","Endocrine cells","Biology","Life Sciences"],"dc:title":["cAMP and Calcium Interactions in Endocrine Cells"],"thesis:degree_level":["Masters Thesis"],"thesis:degree_name":["M.S."]},"updated_at":"2026-07-24T02:03:03Z"}