Developmental changes of glucocorticoid receptors in the rat pancreas

Glucocorticoids are known to play a role in the maturation of the exocrine pancreas. The exact mechanism of glucocorticoid action in pancreatic ontogeny is, however, not clear. The present study characterized and quantitated the binding of [3H]dexamethasone to cytosol fractions from pancreata of rats at various ages. Trunk blood samples from these rats were also checked for levels of free and bound corticosterone. Specific and saturable bindings for dexamethasone were found in pancreatic cytosol fractions from newborn suckling and adult rats. Competition studies showed a preference for steroids with glucocorticoid activity. Specific binding was relatively low in pancreatic cytosol from newly born and 1-day old pups. A significant rise was seen after day 15. Cytosolic binding capacities were greatest from pancreata obtained from pups at weaning (3rd to 5th weeks). Values then declined toward the adult level. Scatchard analysis revealed a single class of binding sites with a dissociation constant (Kd) of 7.3 (+/- 1.1) X 10(-8) M and number of binding sites equalled to 1.29 (+/- 0.18) X 10(-13) mole/mg of cytosolic protein in adult rat pancreas. Pancreata from 25- and 15-day old rats had Kds of 3.4 (+/- 0.8) X 10(-8) M and 2.7 (+/- 0.7) X 10(-8) M with the number of binding sites equal to 1.77 (+/- 0.21) X 10(-13) mole/mg protein and 1.31 (+/- 0.16) X 10(-13) mole/mg protein respectively. Total plasma corticosterone concentration was low before day 10. It rose significantly by day 15, peaked at day 25, and then declined after weaning. About 5-15% of corticosterone during weaning and about 20-30% before and after weaning were in the free form. The peak level of dexamethasone binding corresponded to an increase in the plasma corticosterone level during weaning. This suggests a close relationship between plasma corticosterone levels and pancreatic glucocorticoid receptors. Both may, therefore, play a role in pancreatic development in the rat.     

Influence of GATC sequences on Escherichia coli DNA mismatch repair in vitro.

The effect of the number and position of DNA adenine methylation (dam) sites, i.e., d(GATC) sequences, on mismatch repair in Escherichia coli was investigated. The efficiency of repair was measured in an in vitro assay which used an f1 heteroduplex containing a G/T mismatch within the single EcoRI site. Both an increase in the number of dam sites and a shortened distance between dam site and mismatched site increased the efficiency of mismatch repair. The sequences adjacent to d(GATC) also affected the efficiency of methylation-directed mismatch repair. Furthermore, heteroduplexes with one extra dam site located close to either the 5' or 3' end of the excised base increased the repair efficiency to about the same extent. The findings suggest that the mismatch repair pathway has no preferred polarity.     

脑室注射P物质对大鼠血压、心率及交感传出活动的影响

给乌拉坦麻醉六鼠侧脑室注射P物质(SP)10μg,引起动脉血压、心率和内脏交感神经放电增加。同样剂量的SP静脉注射后却引起血压降低。阿托品预处理不影响SP的开心率作用。预先脑室注射0.25,4,64μg阿片受体拮抗剂纳洛酮,对SP的升压效应有剂量依赖式对抗作用。以上说明脑室注射SP 引起的血压升高是交感神经活动增强,导致心率加快及外周血管紧张性增加的结果,并提示SP的中枢升压效应可能与脑内释放内源性阿片样物质有关。     

溴氰菊酯中毒引起家蝇神经系统环腺苷酸(cAMP)含量的改变

环腺苷酸(cAMP)可在神经传递物刺激腺苷酸环化酶的作用下产生,而坏腺苷酸又可促成神经传递物的产生.用溴氰菊酯(deltamethrin)处理家蝇后,发现酪胺大量增加,主要由于酪氨酸脱羧酶受到诱导、活性增高所致.处理后一小时,cAMP也有增加,并与酶活性的增加相平行,但酪氨酸脱羧酶活性增高的曲线与cAMP量增加的曲线,实际上并不平行,因酪氨酸脱羧酶的活性是先增加,然后下降,而cAMP的量则是在开始时有一个小的下降,接着一直上升,而此时酶的诱导已下降,cAMP含量在诱导开始时出现下降的原因尚不明,可能与环鸟苷酸(cGMP)有关.但随后的上升显然是由于酪胺或章鱼胺的增加所造成.目前已证实,酪胺可经β-羟化作用形成章鱼胺,后者再刺激章鱼胺受体,而使腺苷酸环化酶活化,产生大量的cAMP.酪胺本身也可能就是章鱼胺受体的激活剂.