Stress triggers release of ACTH (adrenocorticotropic hormone) from the pituitary, glucocorticoids from the adrenal cortex, and epinephrine from the adrenal medulla. Though functions differ, these hormone systems interact in many ways. Prior evidence indicates that pituitary and steroid hormones regulate alternative splicing of the Slo gene at the ‘STREX’ exon, 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 (SHRP) 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-day postnatal animals increased the percentage of Slo transcripts with STREX, whereas 20 µM CORT reduced STREX representation. Applied to adrenal chromaffin cells, 20 µM CORT decreased STREX inclusion, whereas neither 500 nm nor 2 µM had any effect. The mineralocorticoid receptor antagonist RU28318 abolished the effect of 500 nm CORT on splicing in pituitary cells, while the glucocorticoid receptor antagonist RU38486 blocked the effect of 20 µM CORT on adrenal chromaffin cells. These results support the hypothesis that the abrupt, transient drop in CORT during the SHRP drives the transient decline in STREX splice variant representation in pituitary, but not adrenal.