Abstract：
:The purpose of this experiment was to determine whether increased secretion of somatostatin or alterations in its molecular form contribute to the age-related decline in growth hormone secretion. Median eminences were removed from male Sprague-Dawley rats (3-4 and 21-24 months of age) and superfused with Krebs-Ringer bicarbonate buffer with 0.5 mg/ml bacitracin. After 40 min, tissues were stimulated with 55 mM K+ for 5 min and fractions collected for 60 min. Tissue and superfusate were analyzed for somatostatin using a highly specific antiserum which cross-reacts with somatostatin-14 and -28. Somatostatin release was expressed as a fractional efflux of somatostatin tissue content. In young rats, somatostatin increased from basal levels of 22 +/- 5 X 10(-4) to 57 +/- 3 X 10(-4) in response to 55 mM K+ and returned to basal levels. Old rats exhibited similar basal levels of somatostatin efflux (25 +/- 5 X 10(-4)) but increased to 91 +/- 19 X 10(-4) in response to K+. This represents an 89% greater increase in somatostatin fractional efflux in old as compared to young rats (P less than 0.05). The molecular form of somatostatin released during K+ stimulation was determined by fractionating samples on Sephadex G-25. In young animals, both somatostatin-14 (31% of total immunoreactivity) and somatostatin-28 (69% of total immunoreactivity) were released by hypothalamic neurons. In old rats, similar absolute levels of somatostatin were released in response to K+ but greater quantities of somatostatin-28 (87% of total immunoreactivity) were secreted.(ABSTRACT TRUNCATED AT 250 WORDS)
journal_name
Brain Resjournal_title
Brain researchauthors
Sonntag WE,Gottschall PE,Meites Jdoi
10.1016/0006-8993(86)90217-9subject
Has Abstractpub_date
1986-08-20 00:00:00pages
229-34issue
2eissn
0006-8993issn
1872-6240pii
0006-8993(86)90217-9journal_volume
380pub_type
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