PubMed · 6149654
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O K Khmel'nitskiĭ, V N Vasil'ev, I I Grintsevich, A A Cheremnykh. 1984. [Thymic carcinoids].. https://pubmed.ncbi.nlm.nih.gov/6149654/
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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.
Lines of rats selectively bred for amygdala excitability, as reflected by kindling rates in response to electrical stimulation, also exhibit differences in tests of anxiety. Inasmuch as corticotropin-releasing hormone (CRH) and bombesin (BN) have been associated with anxiety, regional levels and release of these peptides, as well as plasma adrenocorticotropic hormone (ACTH) and corticosterone, were assessed in 'Slow' and 'Fast' seizing rats following predator exposure (ferret) or immobilization. Ferret exposure elicited a greater increase of plasma ACTH and corticosterone concentrations in the Slow than in the Fast rats. In contrast, immobilization provoked a greater rise of plasma ACTH levels in the Fast rats, paralleling the vigorous struggling observed in this line. In Slow rats, stressor exposure elicited increased levels of ir-BN at the anterior hypothalamus, and increased ir-CRH at the median eminence/arcuate nucleus (Me/Arc), paraventricular hypothalamic nucleus (PVN) and pituitary (Pit), whereas decreased levels of ir-BN were found at the nucleus tractus solitarius (NTS). Fast rats likewise showed decreased ir-BN at the NTS, but unlike the Slow rats, ir-CRH was reduced in the Me/Arc, PVN and Pit in response to both stressors. In vivo microdialysis experiments revealed that in response to ferret exposure, the Slow rats showed a greater CRH release at the central nucleus of the amygdala (CeA) as compared to Fast rats. However, immobilization elicited a more pronounced release of CRH in Fast than in Slow rats. Taken together, the results demonstrate that these two lines of rats show differential endocrinological and neurochemical response patterns to these stressors.
Corticotropin-releasing hormone (CRH) is a neuropeptide thought to play a role in appetite regulation. In this report, we used a serial cerebrospinal fluid (CSF) sampling technique to examine the relationship between CSF CRH, plasma ACTH and cortisol and perceptions of hunger and satiety in fasting and sated volunteers. CSF was withdrawn continuously from 11:00 AM to 5:00 PM via an indwelling subarachnoid catheter. Blood was withdrawn every 10 min via an antecubital vein catheter. Fed subjects received a meal at 1:00 PM. Subjects who were fed had lower post-prandial ratings on hunger scales and higher ratings on satiety scales. Fed subjects also had slightly lower levels of CSF CRH after feeding. Furthermore, fed subjects had higher ACTH and cortisol concentrations in the first 3 h; by the fourth h the opposite was true. Our findings do not support the hypothesis that CNS CRH is a central satiety factor in the human. Instead our findings of slightly diminished CSF CRH levels after feeding may be accounted for by the rises in glucocorticoids and their associated negative feedback effects on CNS CRH. Alternatively, our findings could also reflect changes in CRH levels associated with feeding in multiple brain areas and in the spinal cord with the net effect being in the negative direction.