It is well known that adverse life events can trigger or worsen depression. It has been reported abnormal brain oscillation in depression and also hypothesized that at least, in part, this abnormal brain oscillation might share some features with the neurophysiology of epilepsy.
Are there any connections between reduced serotonin levels, adverse life events, and abnormal brain oscillations?
https://figshare.com/articles/A_neurophysiological_hypothesis_of_how_adverse_life_events_convert_into_abnormal_brain_oscillations_focus_on_unipolar_depression_and_bipolar_disorder/4233002
Dear Amilcar! You talk in a promising direction. Please study the two research articles in the appendix. These articles will help you develop your ideas further. The author of an article draws attention to the role of the large pool of serotonin in the body (gastrointestinal tract).
Vladimir
Dear Vladimir! Thank you very much for your words and reference suggestions. I will read the papers and then I'll give a feedback.
Best regards,
Amilcar
Dear Amilcar:
Literature shows the involvement of dysfunction in CNS serotonergic circuits in the pathophysiology of depression (unipolar depressive disorder or bipolar disorder). Adverse life events and serotonin transporter gene polymorphism have been reported to influence the depressive symptoms in late adulthood. Hence, altered serotonin levels may influence the brain oscillatory activity leading to depression and other mood disorders. The drugs altering serotonin levels are employed for the treatment of depressions and related disorders.
Zahir
I think the adverse life events cause lower serotonin levels in brain by overstimulation of dACC, anterior insula (AI) and amygdala. The dACC and AI activate lateral habenula, which consequently suppresses serotonin release in DRN and MRN. Low MRN serotonin release in the brain leads to abnormal brain oscillations by suppressing slow wave sleep and replay/consolidation of memories and restoration of body during sleep.
So chronic stress and pain and loss and despair would suppress serotonin in brain and also diminish the SWS and SWS linked oscillations. MRN serotonin attenuates theta states = active wakefulness and REM sleep, and theta promoting brain systems attenuate SWS.
In addition overactivation of dACC when we do worry suppresses vACC. My idea is that vACC/BA25 directly stimulates DRN to release serotonin when things go well, when we reach biological and social rewards, safety, good prospects, gain nurture affection and care, get accepted or when we reach our goals and do something well. So high vACC activity promotes well-being and satisfaction and confidence, resilience (to stressors and adversities) and rest. And vACC competes with dACC. dACC hyperstimulation leads to suppression of vACC and consequently to lower DRN serotonin release , while vACC hyperstimulation (i.e. by deep brain stimulation) leads to feeling lighter, less down (at ease, in peace) and ameliorates deprivations, anxieties, fear, anger (vACC reciprocally inhibits CeA) and motivation/drive (when full and satisfied the motivaiton drops by serotonin release at ventral striatum, where it suppresses dopamine release).
Dear Karin Vadovicova.
Thank you for your answer and suggestion.
Best regards.
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