The brain is the key organ of the response to stress. It reacts in a complex, orchestrated manner that is related to the activation / inhibition of structures involved in sensory, motor, autonomic, cognitive and emotional processes. Thus, the brain finally determines what is threatening and, therefore, potentially stressful, as well as the physiological and behavioral responses which can be either adaptive or maladaptive.

Within the brain neuronal circuits that respond to stress are strongly dependent on the type of stressor. Even in the mature differentiated central nervous system neurons and glia cells undergo permanent dynamic changes. The resulting structural plasticity of the brain, its ability to change and to respond reversibly to environmental challenges has been exemplified on the hippocampal formation, a brain structure important for learning, memory, emotional processing, and involved in the control of vegetative and autonomic circuits. The effects of stress on the hippocampal formation seem to range from initial deficits in cognitive and memory function, possibly mediate by a significant and reversible retraction of apical dendrites of pyramidal neurons in the CA3 region, to an increased vulnerability to metabolic insults, reduced neurogenesis and reversible reduction of the hippocampal volume as a whole.

The effects of stress on central nervous processes in non-human primates are demonstrated by studies performed in marmoset monkeys antenatally over-exposed to the synthetic glucocorticoid hormone dexamethasone and in rhesus monkeys derived from stress pregnancies. Our findings indicate that the prenatal environment affects behavior, dysregulates neuroendocrine systems, and influences the brain (hippocampus) of non-human primates.

The immune system is the major defence system in vertebrates, fighting bacterial, viral, and parasite infection. However, the immune system does not only react to pathogens but is also very sensitive to many other environmental influences. During the past three decades, it became increasingly clear that also social and non-social stressors can substantially alter the activity of the immune system in mammals. The highly complex immune system consists of innate and adaptive, as well as of humoral and cellular components. These various levels are an important aspect for stress studies, since a certain stressor can have a quite differential impact on different immune subsystems. Acute social stress in rodents, for example, often suppresses specific immune functions such as the ability of lymphocytes to react to an external challenge (e.g. lymphocyte proliferation), while in contrast, many aspects of the innate immunity such as numbers of granulocytes in the blood and phagocytic activity are often enhanced under these conditions.
Primarily based on examples of small mammals, I shall illustrate (1) some of the typical effects of social stressors on the immune system in wild and captive animals, (2) the modulatory role of individual factors such as previous experience on the immunological outcome, (3) main principles of the underlying neuroendocrine-immune network, and (4) the potential consequences of stress-induced immune modulation for disease susceptibility.
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