Learning achievement, social adjustment, and family conflict among Bedouin-Arab children from polygamous and monogamous families

A sample of 146 Bedouin-Arab pupils from polygamous and monogamous families participated in this study, which was conducted in a Bedouin-Arab village in the Negev, Israel. The authors compared learning achievement, social adjustment, and family conflict. Data revealed differences between the two groups: The children from monogamous families had higher levels of learning achievement than did the children from polygamous families; in addition, those from monogamous families adjusted to the school framework better than did those from polygamous families. The mean conflict rating of children from polygamous families was higher than that of their counterparts from monogamous families. The father's level of education tended to be inversely correlated with family size in terms of both number of children and number of wives.     

Connectionist simulation of attitude learning: asymmetries in the acquisition of positive and negative evaluations

Connectionist computer simulation was employed to explore the notion that, if attitudes guide approach and avoidance behaviors, false negative beliefs are likely to remain uncorrected for longer than false positive beliefs. In Study 1, the authors trained a three-layer neural network to discriminate "good" and "bad" inputs distributed across a two-dimensional space. "Full feedback" training, whereby connection weights were modified to reduce error after every trial, resulted in perfect discrimination. "Contingent feedback," whereby connection weights were only updated following outputs representing approach behavior, led to several false negative errors (good inputs misclassified as bad). In Study 2, the network was redesigned to distinguish a system for learning evaluations from a mechanism for selecting actions. Biasing action selection toward approach eliminated the asymmetry between learning of good and bad inputs under contingent feedback. Implications for various attitudinal phenomena and biases in social cognition are discussed.     

Chronic stress accelerates atherosclerosis in the apolipoprotein E deficient mouse

Conventional cardiovascular risk factors such as cholesterol and blood pressure do not account fully for variation in coronary heart disease suggesting the involvement of additional mechanisms. We have examined the effects of a chronic psychological stress protocol on the development of atherosclerosis in the apolipoprotein E knockout mouse. We observed a 3-fold increase in staining for atheroma accompanied by a 10-fold increase in corticosterone concentrations in mice stressed for 12 weeks. These data suggest that chronic mild stress can induce or accelerate the development of atherosclerosis.     

Fluoxetine inhibits corticotropin-releasing factor (CRF)-induced behavioural responses in rats

Corticotropin-releasing factor (CRF) is a potent neuromodulator of stress-related behaviour but the neural mechanisms underlying these effects are not clear. Studies were designed to test the hypothesis that CRF-induced behavioural arousal involves interactions with brainstem serotonergic systems. To examine interactions between CRF and serotonergic systems in the regulation of behaviour, CRF (1 microg, intracerebroventricular (i.c.v.)) or vehicle was infused in the presence or absence of the selective serotonin re-uptake inhibitor fluoxetine (0, 0.1, 1 or 10 mg/kg, intravenous (i.v.)). Fluoxetine was used at these doses because it is known to decrease serotonin cell firing rates while increasing extracellular serotonin concentrations in select forebrain regions. We then measured behavioural, neurochemical and endocrine responses. CRF increased locomotion and spontaneous non-ambulatory motor activity (SNAMA) in the home cages. Fluoxetine decreased tissue 5-hydroxyindoleacetic acid concentrations, a measure of serotonin metabolism, in specific limbic brain regions of CRF-treated rats (nucleus accumbens shell region, entorhinal cortex, central nucleus of the amygdala). Furthermore, fluoxetine inhibited CRF-induced SNAMA. CRF and fluoxetine independently increased plasma corticosterone concentrations, but the responses had distinct temporal profiles. Overall, these data are consistent with the hypothesis that CRF-induced facilitation of behavioural activity is dependent on brainstem serotonergic systems. Therefore, fluoxetine may attenuate or alleviate some behavioural responses to stress by interfering with CRF-induced responses.     

Is an epigenetic switch the key to persistent extinction?

Many studies of learning have demonstrated that conditioned behavior can be eliminated when previously established relations between stimuli are severed. This extinction process has been extremely important for the development of learning theories and, more recently, for delineating the neurobiological mechanisms that underlie memory. A key finding from behavioral studies of extinction is that extinction eliminates behavior without eliminating the original memory; extinguished behavior often returns with time or with a return to the context in which the original learning occurred. This persistence of the original memory after extinction creates a challenge for clinical applications that use extinction as part of a treatment intervention. Consequently, a goal of recent neurobiological research on extinction is to identify potential pharmacological targets that may result in persistent extinction. Drugs that promote epigenetic changes are particularly promising because they can result in a long-term molecular signal that, combined with the appropriate behavioral treatment, can cause persistent changes in behavior induced by extinction. We will review evidence demonstrating extinction enhancements by drugs that target epigenetic mechanisms and will describe some of the challenges that epigenetic approaches face in promoting persistent suppression of memories.