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.     

Toward an Integration of Interpersonal Risk Models of Depression and Cognitive‐Behaviour Therapy

Empirical research has increasingly focused on interpersonal variables associated with the development and maintenance of depression. This article outlines some key interpersonal risk factors for depression, including anxious attachment, sociotropy, excessive reassurance seeking, interpersonal stress generation, reduced social support, social skills deficits, and social avoidance. Recommendations are made for how cognitive‐behavioural therapy may be adapted to address such factors. Specifically, suggestions are offered for how cognitive and behavioural interventions, such as cognitive restructuring, behavioural activation, behavioural experiments, and skills training, may be used with depressed clients to promote positive relationships and reduce maladaptive interpersonal behaviours.     

Effect of MAO A deficiency on different kinds of aggression and social investigation in mice

Monoamine oxidase A (MAO A) degrades serotonin, dopamine and noradrenaline, factors critically involved in the regulation of aggression. Different kinds of aggression were investigated in Tg8, a transgenic mouse strain lacking a functional MAO A gene. MAO A-deficient mice differ from wild-type C3H/HeJ (C3H) in terms of showing higher territorial, predatory and isolation-induced aggression. Tg8 demonstrated shorter latencies to cricket killing and to the first attack after 6 weeks isolation than C3H mice. In the resident-intruder paradigm, MAO A-lacking mice were more aggressive than C3H when tested as intruders. In contrast to C3H, attack in Tg8 mice did not depend on different aggressiveness of intruders of BALB/c, A/Sn and C3H strains. Tg8 mice displayed no increase in aggression but demonstrated reduced social investigation towards anesthetized, as well as towards juvenile BALB/c males. Thus, MAO A deficiency in Tg8 mice is accompanied by increased expression of different kinds of aggression, as well as by disruption of normal pattern of social interaction.     

Collective Apologies and Their Effects on Forgiveness: Pessimistic Evidence but Constructive Implications

In the last three decades, there has been an explosion in the frequency with which leaders of groups have issued official apologies for collective transgressions. These apologies are commonly assumed to lay a pathway to forgiveness and reconciliation, but empirical examination of the downstream consequences of collective apologies is still in its infancy. In this article, we review a series of studies—including interview studies, survey studies, and experiments—that question the assumed wisdom that collective apologies lead to intergroup forgiveness. Reasons for the muted evidence of an apology–forgiveness link at the intergroup level are elaborated, and implications for how best to issue gestures of reconciliation and remorse are discussed.     

Expansion of Genetic Services Utilizing a General Genetic Counseling Clinic

We established a general genetic counseling clinic (GCC) to help reduce long wait times for new patient appointments and to enhance services for a subset of patients. Genetic counselors, who are licensed in Tennessee, were the primary providers and MD geneticists served as medical advisors. This article describes the clinic referral sources, reasons for referral and patient dispositions following their GCC visit(s). We obtained patients by triaging referrals made to our medical genetics division. Over 24 months, our GCC provided timely visits for 321 patients, allowing the MD geneticists to focus on patients needing a clinical exam and/or complex medical management. Following their GCC visit(s), over 80 % of patients did not need additional appointments with an MD geneticist. The GCC allowed the genetic counselor to spend more time with patients than is possible in our traditional medical genetics clinic. Patient satisfaction surveys (n?=?30) were very positive overall concerning the care provided. Added benefits for the genetic counselors were increased professional responsibility, autonomy and visibility as health care providers. We conclude that genetic counselors are accepted as health care providers by patients and referring providers for a subset of clinical genetics cases. A GCC can expand genetic services, complement more traditional genetic clinic models and utilize the strengths of the genetic counselor health care provider.