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  • Title: Pertussis toxin actions on the pituitary-derived 235-1 clone: effects of PGE1, cholera toxin, and forskolin on cyclic AMP metabolism and prolactin release.
    Author: Cronin MJ, Myers GA, MacLeod RM, Hewlett EL.
    Journal: J Cyclic Nucleotide Protein Phosphor Res; 1983; 9(3):245-58. PubMed ID: 6199389.
    Abstract:
    Pertussis toxin (PT) modulation of the cyclic AMP (cAMP) accumulation induced by prostaglandin E1 (PGE1), cholera toxin (CT), and forskolin was used to study the role of cAMP in the regulation of prolactin release. The clonal cell line 235-1, derived from a rat anterior pituitary tumor, served as the major target tissue. While PT had no effect on basal cAMP levels, in the presence or absence of a phosphodiesterase inhibitor, this novel bacterial toxin potentiated the cAMP response to each stimulus. The PT enhancement of PGE1-stimulated cAMP production was maximal after 24 hr of PT exposure, whether the toxin was left in the medium or removed after as little as 30 sec. Although PGE1, CT, and forskolin are all secretagogues for prolactin, increasing release by about 50%, PT had no apparent effect on these responses. These data support the hypothesis that cAMP may facilitate prolactin release, but may not be the primary stimulus for secretion.
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