Academic stress and personality interact to increase the neural response to high-calorie food cues.

Psychosocial stress is associated with an increased intake of palatable foods and weight gain in stress-reactive individuals. Personality traits have been shown to predict stress-reactivity. However, it is not known if personality traits influence brain activity in regions implicated in appetite control during psychosocial stress. The current study assessed whether Gray's Behavioural Inhibition System (BIS) scale, a measure of stress-reactivity, was related to the activity of brain regions implicated in appetite control during a stressful period. Twenty-two undergraduate students participated in a functional magnetic resonance imaging (fMRI) experiment once during a non-exam period and once during final exams in a counter-balanced order. In the scanner, they viewed food and scenery pictures. In the exam compared with the non-exam condition, BIS scores related to increased perceived stress and correlated with increased blood-oxygen-level dependent (BOLD) response to high-calorie food images in regions implicated in food reward and subjective value, such as the ventromedial prefrontal cortex, (vmPFC) and the amygdala. BIS scores negatively related to the functional connectivity between the vmPFC and the dorsolateral prefrontal cortex. The results demonstrate that the BIS trait influences stress reactivity. This is observed both as an increased activity in brain regions implicated in computing the value of food cues and decreased connectivity of these regions to prefrontal regions implicated in self-control. This suggests that the effects of real life stress on appetitive brain function and self-control is modulated by a personality trait. This may help to explain why stressful periods can lead to overeating in vulnerable individuals.

Maternal factors and monoamine changes in stress-resilient and susceptible mice: cross-fostering effects.

Genetic factors influence stressor-provoked monoamine changes associated with anxiety and depression, but such effects might be moderated by early life experiences. To assess the contribution of maternal influences in determining adult brain monoamine responses to a stressor, strains of mice that were either stressor-reactive or -resilient (BALB/cByJ and C57BL/6ByJ, respectively) were assessed as a function of whether they were raising their biological offspring or those of the other strain. As adults, offspring were assessed with respect to stressor-provoked plasma corticosterone elevations and monoamine variations within discrete stressor-sensitive brain regions. BALB/cByJ mice demonstrated poorer maternal behaviors than C57BL/6ByJ dams, irrespective of the pups being raised. In response to a noise stressor, BALB/cByJ mice exhibited higher plasma corticosterone levels and elevated monoamine turnover in several limbic and hypothalamic sites. The stressor-provoked corticosterone increase in BALB/cByJ mice was diminished among males (but not females) raised by a C57BL/6ByJ dam. Moreover, increased prefrontal cortical dopamine utilization was attenuated among BALB/cByJ mice raised by a C57BL/6ByJ dam. These effects were asymmetrical as a C57BL/6ByJ mice raised by a BALB/cByJ dam did not exhibit increased stressor reactivity. It appears that stressors influence multiple neurochemical systems that have been implicated in anxiety and affective disorders. Although monoamine variations were largely determined by genetic factors, maternal influences contributed to stressor-elicited neurochemical changes in some regions, particularly dopamine activation within the prefrontal cortex.

Parental bonding and depressive affect: the mediating role of coping resources.

Ordinarily, when stressors are encountered, a cascade of cognitive and behavioural responses is evoked that serves to protect the individual from compromised well-being. When coping resources or skills are limited or ineffective, then psychological disturbances, such as depression, may ensue (Paykel, 2001). Although any number of factors could account for variations of stress resilience, this paper argues that early life experiences and relationships, and particularly those with parents or primary caregivers, may contribute to the development of appropriate styles of coping, which, in turn, influence affective responses in the face of stressors encountered in adulthood.

Impact of chronic intermittent challenges in stressor-susceptible and resilient strains of mice.

BACKGROUND: Stressors promote altered neurochemical functioning that may be of adaptive value. The sustained elevations of neurochemical activity elicited by chronic stressors may exact excessive demands on biological systems (allostatic load), thereby rendering the organism more vulnerable to pathology, but such effects may be dependent on individual characteristics. METHODS: Stressor reactive BALB/cByJ mice and the relatively resilient C57BL/6ByJ mice were exposed to a variety of psychogenic and neurogenic stressors, twice a day over 60 days. The resultant neurochemical and behavioral changes in these strains was assessed relative to the effects of acute stressors. RESULTS: Acute restraint elicited more pronounced and more widespread variations of norepinephrine and serotonin utilization in BALB/cByJ than in C57BL/6ByJ mice. Following the chronic stressor, BALB/cByJ mice showed marked behavioral alterations thought to be indicative of depression- and anxiety-like states. The chronic stressor was also associated with moderation of amine utilization in the C57BL/6ByJ mice, whereas such an outcome was less prominent or entirely absent in BALB/cByJ mice. CONCLUSIONS: The sustained increase of amine activity in the BALB/cByJ, coupled with the marked depressionogenic-anxiogenic characteristics of this strain, may provide a useful preparation to assess the impact of chronic stressors on the development of behavioral and physical pathology.

Impact of life-long macronutrient choice on neuroendocrine and cognitive functioning in aged mice: differential effects in stressor-reactive and stressor-resilient mouse strains.

Nutrient selection emerges as a result of both genetic and environmental factors and may be further modified by stressors. The impact of this complex interrelationship on pathological outcomes is poorly understood. In the present investigation the stressor-reactive BALB/cByJ and the relatively stressor resilient C57BL/6ByJ mice were maintained on a macronutrient selection protocol or given free access to chow for 20 months. The C57BL/6ByJ mice exhibited a marked preference for fat over carbohydrates, whereas BALB/cByJ mice preferred carbohydrates over fat. Cognitive testing in a Morris water maze indicated that while BALB/cByJ mice were clearly more impaired in this task relative to their C57BL/6ByJ counterparts, there was no substantial effect of the diet at either 13 or 19 months of age. Furthermore, despite their stressor resiliency, at 19 months of age, C57BL/6ByJ mice who invariably consumed fat, exhibited greater plasma corticosterone responses to a 20-min period of restraint than chow fed animals. Indeed, the corticosterone rise was as pronounced as in the more reactive BALB/cByJ strain. Furthermore, the C57BL/6ByJ diet-fed mice showed features of insulin insensitivity and increased adiposity. These data suggest that the adverse effects of fat consumption need to be considered in the context of genetically determined vulnerability/resilience factors.

An acute psychosocial stress enhances the neural response to smoking cues.

Stress plays an important role in drug addiction. It can trigger relapse in abstinent addicts, and both in the everyday world and in the laboratory, a stressor can induce drug craving. Drug cues, such as the sight of drug, can also trigger subjective craving and relapse, and this effect may be amplified by stress. Underpinning this interaction may be the fact that stress and reward-predicting drug cues act on overlapping brain regions. We exposed 15 smokers undergoing functional magnetic resonance imaging to a psychosocial stressor, the Montreal Imaging Stress Task, followed by drug cues consisting of video clips of smokers. In a separate session similar video clips were shown after a non-stress control task. We observed significantly decreased neural activity during stress in the hippocampus, amygdala, bed nucleus of the stria terminalis, hypothalamus and nucleus accumbens. Following stress there was an increased neural response to drug cues in the medial prefrontal cortex, posterior cingulate cortex, dorsomedial thalamus, medial temporal lobe, caudate nucleus, and primary and association visual areas. These regions are thought to be involved in visual attention and in assigning incentive value to cues. Stress-induced limbic deactivation predicted subsequent neural cue-reactivity. We suggest that stress increases the incentive salience of drug cues.