Abstract
Stressful events, similar to abused drugs, significantly affect the homeostatic balance of the catecholamine brain systems while activating compensation mechanisms to restore balance. In detail, norepinephrine (NE)- and dopamine (DA)-containing neurons within the locus coeruleus (LC) and ventral tegmental area (VTA), are readily and similarly activated by psychostimulants and stressful events involving neural processes related to perception, reward, cognitive evaluation, appraisal, and stress-dependent hormonal factors. Brain catecholamine response to stress results in time-dependent regulatory processes involving mesocorticolimbic circuits and networks, where LC-NE neurons respond more readily than VTA-DA neurons. LC-NE projections are dominant in controlling the forebrain DA-targeted areas, such as the nucleus accumbens (NAc) and medial pre-frontal cortex (mPFC). Heavy and persistent coping demand could lead to sustained LC-NE and VTA-DA neuronal activity, that, when persisting chronically, is supposed to alter LC-VTA synaptic connections. Increasing evidence has been provided indicating a role of autophagy in modulating DA neurotransmission and synaptic plasticity. This alters behavior, and emotional/cognitive experience in response to drug abuse and occasionally, to psychological stress. Thus, relevant information to address the role of stress and autophagy can be drawn from psychostimulants research. In the present mini-review we discuss the role of autophagy in brain catecholamine response to stress and its dysregulation. The findings here discussed suggest a crucial role of regulated autophagy in the response and adaptation of LC-NE and VTA-DA systems to stress.
Highlights
Stress is one consequence of challenges to the organism produced by events known as stressors that are usually identified with stimuli that, by definition, need to be unpredictable, uncontrollable and of forecasting uncertainty
The evidence here discussed points to the remarkable action of autophagy in NE-locus coeruleus (LC) and ventral tegmental area (VTA)-DA connections and its role in NE-dependent neuroprotection, which is crucial for the organism adaptive response to stress and allostatic load
We proposed here the autophagy machinery as a relevant mechanism of regulation and dysregulation of catecholamine neurons
Summary
Stress is one consequence of challenges to the organism produced by events known as stressors that are usually identified with stimuli (or conditions) that, by definition, need to be unpredictable, uncontrollable and of forecasting uncertainty. The occurrence of neural adaptation/maladaptation leads to specific stress-induced alterations of emotion, motivation, cognitive ability and coping In the latter decades, substantial attention has been paid to the role of the autophagy machinery in the physiology of catecholamine brain systems when insulted by pharmacological and neurotoxic agents [51,52,53,54]. The beneficial effects of several antidepressants and mood stabilizers are bound to autophagy activation [57,58,59,60] and autophagy inducers counteract behavioral sensitization induced by abused drugs [51, 56, 61] This wide and prolific research produced results that strongly suggest a crucial role of autophagy in response and adaptation of LC-NE and VTA-DA systems to stress. In the present review we discuss the role of autophagy in brain catecholamine response to stress and those factors which may lead to dysregulation
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