Stress is experienced when stimuli pose a perceived or actual threat to an organism. Exposure to a stressor initiates physiological and behavioral responses that are aimed at restoring homeostasis. In particular, stress activates the hypothalamic-pituitary-adrenal axis, leading to release of glucocorticoids, and engages the autonomic nervous system, causing release of norepinephrine. These “stress hormones” have widespread effects, because most cells express respective receptors that initiate cell-type-specific molecular signaling pathways. In the brain, acute stress promotes neuronal activation, resulting in alertness and adaptive behavioral responses. However, chronic or uncontrolled stress exposure can have deleterious effects on neuronal function, including loss of synaptic connections, which leads to behavioral and cognitive impairments. Stress responses also influence the function of brain-resident microglia and peripheral immune cells that interact with the brain, and alterations in these neuroimmune systems can contribute to the neurobiological and behavioral effects of chronic stress. Ongoing research is aimed at uncovering the molecular and cellular mechanisms that mediate stress effects on neuroimmune systems, and vice versa.
Article
Eric S. Wohleb
Proper immune function is critical to maintain homeostasis, recognize and eliminate pathogens, and promote tissue repair. Primary and secondary immune organs receive input from the autonomic nervous system and immune cells express receptors for epinephrine, norepinephrine, and/or acetylcholine. Through direct signaling the autonomic nervous system controls immune function by altering immune cell development, initiating redistribution of immune cells throughout the body, and promoting molecular pathways that shift immune cell reactivity. This neuroimmune communication allows the autonomic nervous system to shape immune function based on physiological and psychological demands.
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Understanding of the brain mechanisms regulating reproductive behaviors in female laboratory animals has been aided greatly by our knowledge of estrogen receptors in the brain. Hypothalamic neurons that express the gene for estrogen receptor-alpha regulate activity in the neural circuit for the simplest female reproductive response, lordosis behavior. In turn, many of the neurotransmitter inputs to the critical hypothalamic neurons have been studied using electrophysiological and neurochemical techniques. The upshot of all of these studies is that lordosis behavior presents the best understood set of mechanisms for any mammalian behavior.
