Abstract
Neural plasticity plays a critical role in mediating short- and long-term brain responses to environmental stimuli. A major effector of plasticity throughout many regions of the brain is stress. Activation of the locus coeruleus (LC) is a critical step in mediating the neuroendocrine and behavioral limbs of the stress response. During stressor exposure, activation of the hypothalamic-pituitary-adrenal axis promotes release of corticotropin-releasing factor in LC, where its signaling promotes a number of physiological and cellular changes. While the acute effects of stress on LC physiology have been described, its long-term effects are less clear. This review will describe how stress changes LC neuronal physiology, function, and morphology from a genetic, cellular, and neuronal circuitry/transmission perspective. Specifically, we describe morphological changes of LC neurons in response to stressful stimuli and signal transduction pathways underlying them. Also, we will review changes in excitatory glutamatergic synaptic transmission in LC neurons and possible stress-induced modifications of AMPA receptors. This review will also address stress-related behavioral adaptations and specific noradrenergic receptors responsible for them. Finally, we summarize the results of several human studies which suggest a link between stress, altered LC function, and pathogenesis of posttraumatic stress disorder.
Highlights
Stressful stimuli and events engage a number of brain circuits that activate the hypothalamic-pituitary-adrenal (HPA) axis
We have previously shown that both stressor exposure in vivo [62] and corticotropin-releasing factor (CRF) exposure ex vivo [49] alter locus coeruleus (LC) AMPA receptor (AMPAR) signaling
Stressor exposure induces a series of neuroendocrine, physiological, and behavioral adaptations that promote an appropriate response to the stressor
Summary
Stressful stimuli and events engage a number of brain circuits that activate the hypothalamic-pituitary-adrenal (HPA) axis. Using RNA-Seq, we identified that expression of Ntf, the gene for neurotrophin 3, which promotes neuronal survival, differentiation, and neurite outgrowth [18, 90], was approximately twice as high in rats one week after stressor exposure than in their control counterparts (Figure 2) These observations, in combination with earlier reports of stress-induced morphological alterations in LC neurons [50, 52, 53, 75, 91,92,93], suggest that stress may cause long-lasting changes in noradrenergic transmission throughout the CNS in response to even acute stressor exposure. The male and female LC may be differentially aligned to respond to stress with specific neuroplastic adaptations that promote disease
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