Effect of chronic ethanol administration on intermale aggression in rats

An experiment was performed to study the effect of chronic ethanol administration on intermale aggression in rats using a 24-hour resident-intruder test. During the resident-intruder test residents displayed virtually all of the agonistic behaviors, and intruders displayed virtually all of the defensive behaviors. Intruders treated with ethanol displayed more defensive behavior and elicited more agonistic behavior than control intruders. Twenty minutes into the resident-intruder test intruders showed the greatest increase in corticosterone (338% vs. 129%), while residents showed the greatest increase in testosterone (103% vs. 18%). On the 2nd day of the resident-intruder test intruders lost more weight than residents (21.5 g vs. 10.2 g). Plasma corticosterone levels remained elevated for the intruders, and in particular for those intruders displaying defensive behaviors regardless of the resident's behavior. Plasma testosterone levels remained elevated for those residents that were paired with intruders that displayed defensive behaviors regardless of the resident's behavior. The frequency and severity of biting attacks by ethanol residents was significantly greater than that of control residents. In addition, the locus of biting attack shifted from the upper back of intruders paired with control residents to the flanks, tail, lower feet, and ventral surface on intruders paired with ethanol residents.     

Some adrenal correlates of aggression in isolated female mice

Forty-six female mice (CFW) were isolated for a period of 23 weeks. The effect of isolation on fighting behavior was tested weekly by introducing a naive brown female mouse into the subject's home cage. Total leucocyte counts were obtained at 8 and 14 weeks of isolation. The appearance of leucopenia was used as an index of elevated adrenocortical activity. After 23 weeks of isolation all animals were sacrificed by decapitation. Plasma was collected for corticosterone assay, and paired adrenals were used to assay catecholamine levels. On the basis of the frequency and/or the absence of fighting, the mice were segregated into fighters (n = 22) and non-fighters (n = 17). Analysis of the data by Pearson's product moment correlation and Student's t-test showed that elevated sympathetic-adrenal activity was positively correlated with aggression and that elevated adrenocortical activity was negatively correlated with aggression.     

Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval

It is well established that glucocorticoid hormones, secreted by the adrenal cortex after a stressful event, influence cognitive performance. Some studies have found glucocorticoid-induced memory enhancement. However, many studies have reported impairing effects of glucocorticoids on memory function. This paper reviews recent findings from this laboratory on the acute effects of glucocorticoids in rats on specific memory phases, i.e., memory consolidation and memory retrieval. The evidence suggests that the consequences of glucocorticoid activation on cognition depend largely on the different memory phases investigated. Posttraining activation of glucocorticoid-sensitive pathways involving glucocorticoid receptors enhances memory consolidation in a pattern highly similar to that previously described for adrenal catecholamines. Also, similar to catecholamine effects on memory consolidation, glucocorticoid influences on memory consolidation depend on noradrenergic activation of the basolateral complex of the amygdala and interactions with other brain regions. By contrast, memory retrieval processes are usually impaired with high circulating levels of glucocorticoids or following infusions of glucocorticoid receptor agonists into the hippocampus. The hypothesis is proposed that these apparently dual effects of glucocorticoids on memory consolidation and memory retrieval might be related and that the basolateral complex of the amygdala is a key structure in a memory-modulatory system that regulates, in concert with other brain regions, stress and glucocorticoid effects on both memory consolidation and memory retrieval.     

Effects of peripheral immune activation on social behavior and adrenocortical activity in aggressive mice: Genotype-environment interactions

To explore genetic-developmental differences in the biobehavioral effects of induced illness, males from two lines of mice selectively bred for high or low levels of aggressive behavior were injected with endotoxin (Escherichia coli, LPS: 0.25 mg/kg, 1.25 mg/kg, or 2.5 mg, i.p.) or saline. Body temperature, weight, and locomotor activity were monitored immediately before and 8 and 24 hr after injection. Twenty-four hours after injection, social behaviors were assessed in a 10-min dyadic test, and hypothalamus, spleen, and serum were collected. In both lines, endotoxin treatment increased behavioral immobility ("freezing") and decreased social exploration. Other effects showed line differences: Males from the high-aggressive line had a lower threshold to endotoxin-induced effects on body temperature, weight loss, spleen weight, and corticosterone. Social reactivity (startle response to mild social investigation) increased in the high-aggressive line and decreased in the low-aggressive line after treatment. In the high-aggressive line only, endotoxin decreased attack frequency and increased latency to attack. The interactions between selected line (genotype) and endotoxin treatment (environment) demonstrate that genetic-developmental differences in social and aggressive behavior may indicate the extent to which immune stimuli (e.g., bacteria, viruses, cytokines) function as "biobehavioral stressors." Aggr. Behav. 23:93–105, 1997.© 1997 Wiley-Liss, Inc.     

电击信号应激对大鼠体液免疫及内分泌功能的影响

研究了足电击及以电击装置为信号刺激所诱发的情绪应激对大鼠原发性体液免疫反应及内分泌的影响。 结果表明每天１０分钟,共６天的足电击对大鼠抗特异性抗原ＯＶＡ的原发性体液免疫反应无明显作用,而此电击作 用结合每天１０分钟,共８天的情绪应激则可显著降低大鼠体液免疫反应及脾脏指数。同时该应激可显著提高大鼠 血儿茶酚胶和皮质酮水平。该研究证明了情绪应激对大鼠体液免疫功能的调节作用,并对交感神经系统和下丘脑－ 垂体－肾上腺（ＨＰＡ）轴在其中所起的作用进行了初步探讨。     

Reliability of the Chronic Mild Stress paradigm: Implications for research and animal welfare

The Chronic Mild Stress (CMS) model for depression has become central to the empirical literature on depression. There are however inconsistencies in the literature concerning the robustness of the phenomenon of anhedonia following CMS procedures. We report that not only did our procedures (modeled on the original reports) fail to induce an anhedonia, but in fact led to increased sucrose consumption. Furthermore, corticosterone levels following CMS procedures were lower than following control procedures. Given that this is not the first report of such findings, it is important to evaluate whether and which aspects of the experimental methodology are necessary or sufficient to induce the state of anhedonia.     

心理应激的免疫抑制作用及其与神经内分泌反应的相关性

以给予经定时喂水训练大鼠空瓶刺激为情绪性心理应激源,研究了此情绪应激对大鼠特异性原发体液免疫反应的影响及其可能的作用机制。结果表明每次10分钟,共14次的情绪应激显著降低大鼠抗特异性抗原OVA的抗体水平及脾脏指数,而显著增高血肾上腺素、去甲肾上腺素和皮质酮水平。研究还发现去甲肾上腺素与抗特异性抗原OVA的抗体水平呈显著负相关。该研究证实了情绪性心理应激对大鼠体液免疫功能的抑制作用,并提示交感神经系统可能参与了此免疫调节作用。     

Effects of age at differential housing and the duration of individual housing/grouping on lntermale fighting behavior and adrenocortical activity in TO strain mice

A study of the effects of the duration of individual and group housing on intermale fighting and adrenocortical activity was conducted in TO strain mice. It was found that fighting and threat increased with progressive isolation up to an asymptote at 56–58 days. ‘Basal’ adrenocortical function differed little under the 2 housing conditions, but after ‘stress,’ mice isolated for short periods, which had not fought when tested for aggression, had lower titers than group-housed counterparts. However, mice that had been isolated for longer periods, and had fought in aggression tests, had higher corticosterone titers than comparable group-housed animals. The effects of a short duration (28–30 days) of differential housing, commencing at different ages, were also studied. The shorter duration adrenocortical changes were largely confirmed. In general, the earlier the age at which the differential housing was imposed, the greater the behavioral differences between animals under each housing condition. It is suggested that this is largely a consequence of a loss of behavioral plasticity in older mice. The data provides little support for the concept of the “isolation stress syndrome,” or for the view that the characteristic fighting exhibited by individually housed mice is a consequence of “social deprivation”.     

The neurochemistry of pair bonding

The formation and maintenance of social attachments are fundamental to human biology. Because deficits in the ability to form such attachments are associated with a variety of psychological disorders, an understanding of the neural basis of social attachment may provide insights into the causes of such disorders. Comparative studies using several closely related species of voles that display different social organizations and behaviors have begun to provide important insights into the neurochemical events underlying social attachment. Here we review recent developments in the study of social attachment, focusing on the roles of specific neurochemical systems in pair-bond formation.