PubMed · 4300498
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J A Moriarty. 1968. Optic neuritis.. https://pubmed.ncbi.nlm.nih.gov/4300498/
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The endocrine response to stress is an important homoeostatic mechanism, and the secretion of glucocorticoids from the adrenal cortex is a central feature of this response. During early postnatal development, the neonatal rat displays a reduced hypothalamic-pituitary-adrenal (HPA) response to stress. This early period has been termed the 'stress hyporesponsive period' (SHRP). Maternal separation (Sep) of neonates from their mothers during early postnatal development alters the HPA response to stress. In this study, we report the effects of Sep during the SHRP. Female rats were time mated and randomly divided into control or Sep groups before birth. The Sep litters were removed from the mothers during the dark cycle for 6 h per day from postnatal day (PND) 2 to 10. On PND 28, the pups from both groups were weighed, the anogenital distance (AGD) was measured and the animals weaned. At 40 days of age, male and female animals from both groups were tested for open-field activity. As the animals matured, vaginal opening and estrous cycles were measured in females, and males were tested for male sexual behavior at adulthood. Basal, stress, and stress recovery serum corticosterone levels were measured from control and Sep male and female animals. Open-field activity was not significantly different between control or Sep male or female animals. Sep did not affect either vaginal opening or estrous cycles in female animals. Corticosterone secretion in response to stress was similar in control and Sep males and females; however, the recovery levels were significantly higher in Sep females than in Sep males or female control values. In male sexual behavior tests, Sep males had significantly longer mount latencies (time to the first mount), longer intromission latencies (time to the first intromission) and a significant reduction in the percent of animals ejaculating versus control values (controls 84 and Sep 50%). Therefore, Sep males as adults displayed altered reproductive behavior, whereas their stress recovery levels of corticosterone returned to near basal levels in a similar fashion to that observed for control non-handled males. In contrast, females displayed normal reproductive physiology, while their recovery levels of corticosterone remained high, unlike that observed with control females. Thus, significant gender differences in response to Sep (during the dark phase of the circadian cycle) were observed in the paradigm used in the present study.
Administration of adrenocorticotropic hormone (ACTH) has been shown to decrease plasma concentrations of apolipoprotein B (apoB) containing lipoproteins, including lipoprotein(a), in man. However, the mechanism behind this hypolipidemic effect is unknown. This study aimed at distinguishing between the main possibilities (increased elimination or decreased production of lipoproteins) using HepG2 cell cultures. Addition of ACTH to the cell culture medium selectively down-regulated apoB mRNA expression and apoB secretion in a dose-dependent manner. At 100 pmol/liter ACTH, the apoB mRNA level was about 40% lower than in the untreated cells, and the secretion of apoB into the medium was decreased to a similar extent. The expression and secretion of other apolipoproteins (apoA-I, apoE, and apoM), however, were not affected by ACTH. Under normal culture conditions the level of secretion of apoB from HepG2 cells is quite low. In the presence of 0.4 mmol/liter oleic acid secretion of apoB increased 3-fold, but this phenomenon was not seen in ACTH-treated cells. Binding and internalization of radiolabeled low density lipoprotein (LDL) by HepG2 cell, as well as LDL-receptor mRNA and scavenger receptor B-I mRNA levels, were not influenced by ACTH. In conclusion, ACTH directly and selectively down-regulated the production and secretion of apoB in HepG2 cell cultures, suggesting that a principal mechanism behind the cholesterol-lowering effect of ACTH in vivo may be a decreased production rate of apoB-containing lipoproteins from the liver.
para-Chloroamphetamine, an amphetamine analog, alters serotonergic neurochemistry. In previous reports, melatonin (MEL), when administered with other amphetamine analogs, altered the decline in serotonin content produced by these analogs. The present studies assessed the effects of various doses of melatonin and p-chloroamphetamine on serotonin levels in numerous brain regions in male rats. Melatonin (10, 25 or 50 mg/kg, s.c.) and p-chloroamphetamine (3 or 5 mg/kg, s.c.) were administered and, 3 h later, brain samples and serum were collected. Serotonin levels in the serum and various regions of the brain were assayed using high-performance liquid chromatography. Melatonin in combination with a high dose of p-chloroamphetamine (5 mg/kg) produced cumulative deficits in serotonin levels in the serum. However, serotonin levels in the pineal, cortex or brain stem in all combined melatonin and p-chloroamphetamine groups were not significantly different from groups that received p-chloroamphetamine alone. Serum adrenocorticotropin (ACTH) and corticosterone levels were significantly elevated in the melatonin and p-chloroamphetamine combined groups, suggesting that animals receiving both treatments were more stressed than control animals or animals receiving melatonin or p-chloroamphetamine alone. These results indicate that melatonin does not alter p-chloroamphetamine-induced deficits in central serotonin levels. The increased serum adrenocorticotropic hormone, corticosterone and serotonin levels observed following melatonin and p-chloroamphetamine treatment suggest that this combination may have adverse peripheral effects.