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題名 Regulation of alternative splicing of Slo K+ channels in adrenal and pituitary during the stress hyporesponsive period of rat development 作者 賴桂珍
Lai,Guey-Jen;McCobb DP貢獻者 神科所 日期 2006.05 上傳時間 23-Sep-2014 12:26:12 (UTC+8) 摘要 Stress triggers release of ACTH from the pituitary, glucocorticoids from the adrenal cortex, and epinephrine from the adrenal medulla. Although functions differ, these hormone systems interact in many ways. Previous evidence indicates that pituitary and steroid hormones regulate alternative splicing of the Slo gene at the stress axis-regulated exon (STREX), with functional implications for the calcium-activated K+ channels prominent in adrenal medullary and pituitary cells. Here we examine the role of corticosterone in Slo splicing regulation in pituitary and adrenal tissues during the stress-hyporesponsive period of early rat postnatal life. The sharp drop in plasma corticosterone (CORT) that defines this period offers a unique opportunity to test CORT`s role in Slo splicing. We report that in both adrenal and pituitary tissues, the percentage of Slo transcripts having STREX declines and recovers in parallel with CORT. Moreover, addition of 500 nm CORT to cultures of anterior pituitary cells from 13-, 21-, and 30-d postnatal animals increased the percentage of Slo transcripts with STREX, whereas 20 microm CORT reduced STREX representation. Applied to adrenal chromaffin cells, 20 microm CORT decreased STREX inclusion, whereas neither 500 nm nor 2 microm had any effect. The mineralocorticoid receptor antagonist RU28318 abolished the effect of 500 nm CORT on splicing in pituitary cells, whereas the glucocorticoid receptor antagonist RU38486 blocked the effect of 20 microm CORT on adrenal chromaffin cells. These results support the hypothesis that the abrupt, transient drop in CORT during the stress-hyporesponsive period drives the transient decline in STREX splice variant representation in pituitary, but not adrenal. 關聯 Endocrinology,147(8),3961-3967 資料來源 http://dx.doi.org/10.1210/en.2005-1551 資料類型 article dc.contributor 神科所 en_US dc.creator (作者) 賴桂珍 zh_TW dc.creator (作者) Lai,Guey-Jen;McCobb DP en_US dc.date (日期) 2006.05 en_US dc.date.accessioned 23-Sep-2014 12:26:12 (UTC+8) - dc.date.available 23-Sep-2014 12:26:12 (UTC+8) - dc.date.issued (上傳時間) 23-Sep-2014 12:26:12 (UTC+8) - dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/70092 - dc.description.abstract (摘要) Stress triggers release of ACTH from the pituitary, glucocorticoids from the adrenal cortex, and epinephrine from the adrenal medulla. Although functions differ, these hormone systems interact in many ways. Previous evidence indicates that pituitary and steroid hormones regulate alternative splicing of the Slo gene at the stress axis-regulated exon (STREX), with functional implications for the calcium-activated K+ channels prominent in adrenal medullary and pituitary cells. Here we examine the role of corticosterone in Slo splicing regulation in pituitary and adrenal tissues during the stress-hyporesponsive period of early rat postnatal life. The sharp drop in plasma corticosterone (CORT) that defines this period offers a unique opportunity to test CORT`s role in Slo splicing. We report that in both adrenal and pituitary tissues, the percentage of Slo transcripts having STREX declines and recovers in parallel with CORT. Moreover, addition of 500 nm CORT to cultures of anterior pituitary cells from 13-, 21-, and 30-d postnatal animals increased the percentage of Slo transcripts with STREX, whereas 20 microm CORT reduced STREX representation. Applied to adrenal chromaffin cells, 20 microm CORT decreased STREX inclusion, whereas neither 500 nm nor 2 microm had any effect. The mineralocorticoid receptor antagonist RU28318 abolished the effect of 500 nm CORT on splicing in pituitary cells, whereas the glucocorticoid receptor antagonist RU38486 blocked the effect of 20 microm CORT on adrenal chromaffin cells. These results support the hypothesis that the abrupt, transient drop in CORT during the stress-hyporesponsive period drives the transient decline in STREX splice variant representation in pituitary, but not adrenal. en_US dc.format.extent 253153 bytes - dc.format.mimetype application/pdf - dc.language.iso en_US - dc.relation (關聯) Endocrinology,147(8),3961-3967 en_US dc.source.uri (資料來源) http://dx.doi.org/10.1210/en.2005-1551 en_US dc.title (題名) Regulation of alternative splicing of Slo K+ channels in adrenal and pituitary during the stress hyporesponsive period of rat development en_US dc.type (資料類型) article en