INDIVIDUAL COPING STRATEGIES AND VULNERABILITY TO STRESS PATHOLOGY

Psychosocial factors are implicated in the individual development, course and recovery from disease. Studies with animal models using social interactions show that the magnitude and direction of changes in the immune-, neuroendocrine-, and cardiovascular system are highly correlated with the social position of the animal. This relationship appears to depend on the animalxs coping strategy both in terms of behaviour and neuroendocrinology, and hence in immunology as well. It is argued that disease processes should be considered as a function of the baseline behavioural, neuroendocrine, and immunological state

The Corticomedial Amygdala and Learning in an Agonistic Situation in the Rat

Social agonistic behaviour of intact male rats is strongly reduced by the experience of defeat by a dominant male conspecific. Small electrolytic lesions in the corticomedial amygdala strongly affected this behavioural change due to defeat. No effects of the lesions were observed before and during the defeat. Some learning is still possible in corticomedial amygdala lesioned animals. A comparison of the effects of lesions made before the defeat with lesions made after the defeat revealed that the lesions primarily produce a retention deficit in social learning.

Vasopressin Prolongs Behavioral and Cardiac Responses to Mild Stress in Young But Not in Aged Rats

In young male Wistar rats sudden silence superimposed on low intensity background noise evokes a relative decrease in heart rate. This bradycardia is accompanied by immobility behavior. In the present study, involving young (3 month), late-adult (14 month), aged (20 month), and senescent (25 month) rats the magnitude of the stress-induced bradycardia shows an age-related reduction while the behavioral immobility response remained unchanged during the process of aging. Arginine-8-vasopressin (AVP, 6 µg/kg SC) administered 60 min prior to the experiment led to a prolonged behavioral and cardiac stress response in young and late-adult rats, but not in aged and senescent animals. The peripheral and central mechanisms possibly involved in the failure of systemically applied AVP to improve bradycardiac stress responses in aged rats are discussed.

Behavioral and Cardiac Responses to Mild Stress in Young and Aged Rats:Effects of Amphetamine and Vasopressin

Young (3-month-old) male Wistar rats showed a relative decrease in heart rate to a sudden silence superimposed on low intensity background noise. This bradycardia was accompanied by immobility behavior. In 26-month-old rats the magnitude of the heart rate response was reduced while immobility behavior remained in the same order of magnitude as in young controls, in the aged rats a shift in autonomic regulation of heart rate in the direction of increased sympathetic influence was indicated by the results obtained by blocking the autonomic input with atropine methyl-nitrate (0.5 mg/kg) or atenolol (1 mg/kg) given subcutaneously (SC) 30 min prior to testing. Pretest (30 min) administration of amphetamine (0.5 mg/kg SC) reinstated the bradycardiac response in aged rats to a level seen in young ones. Arginine-vasopressin (AVP, 10 µg/kg SC), administered 60 rain before the experiment, markedly facilitated the cardiac response in young animals but failed to restore cardiac responses in aged ones. The immobility behavior in the peptide-treated aged rats was also absent. The present findings suggest that a diminished central aminergic drive in aged rats is causing a reduction of the parasympathetic cardiac response to stress of sudden silence. The results also indicate an age-related vasopressinergic modulation of behavioral and cardiac responses to mild stress