Facing stress.

Schizophrenia is considered a neurodevelopmental disorder in which vulnerability to stress may be a contributing factor. Coping is an important psychological component of stress processing, and the hypothalamic-pituitary-adrenal system (HPA system) is one of the biological components of stress adaptation. Disturbances of either of these components may make schizophrenic patients more vulnerable to develop a psychosis under stressful circumstances. In this study, 10 schizophrenic men were compared with 10 healthy male controls in their response to a psychosocial stressor, consisting of a public-speaking task. Heart rate was monitored as a measure of autonomic arousal. HPA responses were assessed by measuring salivary cortisol. Coping skills were measured by using the Utrecht Coping List and the Ways of Coping Checklist. The stress of speaking in public increased the heart rate in both patients and controls; however, a significant cortisol response was found in the controls, but not in the schizophrenic patients. The patients used more passive and avoidant coping strategies than controls. The findings provide support for the notion that schizophrenic patients have an impaired ability to adapt, both psychologically and biologically, to their environment.

Adaptation, Psychological↗

PubMed1998

Essential role of the fosB gene in molecular, cellular, and behavioral actions of chronic electroconvulsive seizures.

The role of Fos-like transcription factors in neuronal and behavioral plasticity has remained elusive. Here we demonstrate that a Fos family member protein plays physiological roles in the neuronal, electrophysiological, and behavioral plasticity associated with repeated seizures. Repeated electroconvulsive seizures (ECS) induced isoforms of DeltaFosB in frontal cortex, an effect that was associated with increased levels of the NMDA receptor 1 (NMDAR1) glutamate receptor subunit. Induction of DeltaFosB and the upregulation of NMDAR1 occurred within the same neurons in superficial layers of neocortex. Activator protein-1 (AP-1) complexes composed of DeltaFosB were bound to a consensus AP-1 site in the 5'-promoter region of the NMDAR1 gene. The upregulation of NMDAR1 was absent in mice with a targeted disruption of the fosB gene. In addition, repeated ECS treatment caused progressively shorter motor seizures (tolerance) in both rats and wild-type mice, as well as reduced NMDA-induced inward currents in pyramidal neurons from superficial layers of the neocortex of wild-type mice. These behavioral and electrophysiological effects were also significantly attenuated in fosB mutant mice. These findings identify fosB gene products as transcription factors critical for molecular, electrophysiological, and behavioral adaptations to motor seizures.

Adaptation, Psychological↗