An analysis of some sensitizing agents in the pathogenesis of stress-induced gastric erosive disease

Prior surgical implantation of a venous catheter sensitized rats to coldimmobilization stress. Three of six catheterized females succumbed during the stress. The remaining rats fell into two groups in terms of their core temperature at the end of the stress period: Male uncatheterized rats had higher temperatures than rats in the other three groups. No relation was found between catheter patency and magnitude of hypothermia. Degree of gastric disease paralleled the core temperature findings in that the male uncatheterized rats had significantly fewer gastric erosions than the rats in the other three groups. Additionally, a robust effect of gender was found with uncatheterized females showing more hypothermia and more gastric disease than uncatheterized males. A subsequent experiment was conducted to evaluate whether anesthesia or wearing the protective spring was responsible in part for the sensitization seen. Here, the gender difference was less although females consistently averaged lower core temperatures after stress than did males. Despite similar core temperatures after stress, females that were prepared with the protective spring apparatus developed more gastric disease than female controls or similarly treated males. Thus, the additional sensitization exhibited by females in the first experiment may relate to the fact that both catheterization and the taping procedure were sensitizers while only catheterization was a sensitizer for males.     

Inhibition of the LH Surge by Restraint Stress in Cyclic Rats: Studies on the Role of GABAA and GABAB Receptors

There is evidence that stress can alter the activity in the brain of gamma-aminobutyricacid (GABA), a neurotransmitter that has been implicated in the regulation of LH secretion. In the present study the role of GABA in the restraint stress-induced inhibition of the LH surge was investigated in the intact cyclic rat. Intracerebroventricular (icv) administration of the GABAA receptor agonist muscimol (0.1, 0.5 or 1 μg) 5 min before the presumed onset of the pro-oestrous LH surge (at 0900 h) caused a dose dependent suppression of the surge. A single dose of the GABAB receptor agonist baclofen (1 μg; icv) injected at 0855 h postponed the onset of the LH surge, and repeated injections at 0855 and 1130 h suppressed the surge. These data indicate that GABA-ergic activity in the brain can inhibit the LH surge in the cyclic rat via GABAA and GABAB receptors. Pro-oestrous rats were subjected to 5 hrs of restraint starting at 0855 h. Pretreatment with the GABAA receptor antagonist bicuculine (1 μg; icv) at 0840, 0940 and 1040 h or pretreatment with the GABAB receptor antagonist phaclofen (10 μg; icv) at 0840 h were ineffective in preventing the restraint-induced inhibition of the LH surge. The results suggest that GABAA and GABAB receptors are not involved in the inhibitory effect of restraint stress on the LH surge.     

Effects of Acute Stress or Centrally Injected Interleukin-1beta on Neuropeptide Expression in the Immune System

Acute stress stimulates the expression and release of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) from the hypothalamus, and the pro-opiomelanocortin products beta-endorphin and ACTH from the anterior pituitary. These neuropeptides are also expressed in immune tissues, and it has been proposed that they may modulate immune responses to stress through paracrine mechanisms. We subjected rats to restraint stress or central injection of interleukin (IL)-1beta to determine whether these acute stimuli can alter the expression of neuropeptides in the spleen and thymus. Restraint stress significantly increased the contents of all these neuropeptides in thymic, but not splenic, extracts. A single icv injection of IL-1beta increased contents of CRH, AVP, ACTH and beta-endorphin in the spleens of both sham-operated and adrenalectomised (ADX) rats. IL-1beta increased thymic contents of CRH and ACTH in sham-operated rats but these increases were not observed in ADX rats. These results suggest that the effects of IL-1beta on neuropeptide expression in the spleen are independent of glucocorticoids, whereas IL-1beta stimulation of neuropeptide expression in the thymus is dependent on circulating glucocorticoids. There were significant correlations between increases in CRH, ACTH and beta-endorphin in the spleen, and between CRH and ACTH in the thymus, consistent with the suggestion that IL-1beta-induced increases in ACTH and beta-endorphin may be mediated through CRH. These results provide evidence that stressors can directly influence neuropeptide expression in immune tissues. Thus stress may influence immune functions through paracrine mechanisms involving locally synthesised neuropeptides as well as through activation of the hypothalamo-pituitary-adrenal axis.     

大学二年级学生人际宽恕与报复心理及其与抑郁的关系研究

采用沉思量表、报复动机量表、宽恕倾向量表、宽恕态度量表和流调中心用抑郁量表对236名大二学生进行问卷调查,综合探讨大学生人际宽恕和报复心理及其与抑郁的关系。研究发现:(1)男大学生的报复倾向显著高于女大学生。(2)宽恕倾向与报复倾向及对侵犯的沉思程度显著负相关。沉思程度和抑郁显著正相关。(3)沉思程度和宽恕倾向对抑郁分别具有显著的正向和负向的预测作用。(4)大学生的宽恕倾向和宽恕态度的相互作用以及宽恕倾向和报复倾向之间的交互作用对抑郁均没有显著预测作用。     

Information processing bias against emotional facial expressions in social anxiety

The present study examined whether information processing bias against emotional facial expressions is present among individuals with social anxiety. College students with high (high social anxiety group; n  = 26) and low social anxiety (low social anxiety group; n  = 26) performed three different types of working memory tasks: (a) ordering positive and negative facial expressions according to the intensity of emotion; (b) ordering pictures of faces according to age; and (c) ordering geometric shapes according to size. The high social anxiety group performed significantly more poorly than the low social anxiety group on the facial expression task, but not on the other two tasks with the nonemotional stimuli. These results suggest that high social anxiety interferes with processing of emotionally charged facial expressions.