Wellbutrin is an NE and DA reuptake inhibitor. I have used it and the effects on norepinephrine was very stimulating. I had to take the XL at 150 mg. I was on two other meds. at the time and with adjustments it worked well.
Here are links for norepinephrine and one for the pharmacological proprieties of Wellbutrin
https://www.drugs.com/mtm/norepinephrine.html
Wellbutrin XL (Bupropion Hydrochloride Extended-Release): Side Effects, Interactions, Warning, Dosage & Uses
TCAs often cause drowsiness, depending on which one is used and the dose.
Here is a link to Tricyclic antidepressants-
http://www.bpac.org.nz/BPJ/2006/Dece...pages22-23.pdf
Concerning Trazadone (SARI)-
Trazodone was originally supposed to be utilized as a relatively safe anti-depressant. Basically targeting the 5-HT receptors/SERT including the 5HT2C receptor. The problem with Trazadone as an effective antipressant; the therapeutic dose is around 200-300mg. The issue is at that level the anticholgenic makes people very sedated and thus it's use as a conventional SSRI type antidepressant was limited. It has found its niche as an effective and generally safe sleep medication using doses of 25-100mg without the physical tolerance and addictive qualities of the Z drugs and benzodiazepines. These target and bind to the GABA subreceptors. Which will over time increase intolerance as GABA receptors die off unless these meds. are used cautiously for a very short time or a strict prn.
Quote:
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Because of its lack of anticholinergic side effects, trazodone is especially useful in situations in which antimuscarinic effects are particularly problematic (e.g., in patients with benign prostatic hyperplasia, closed-angle glaucoma, or severe constipation). Trazodone's propensity to cause sedation is a dual-edged sword. For many patients, the relief from agitation, anxiety, and insomnia can be rapid; for other patients, including those individuals with considerable psychomotor retardation and feelings of low energy, therapeutic doses of trazodone may not be tolerable because of sedation. Trazodone elicits orthostatic hypotension in some patients, probably as a consequence of α1-adrenergic receptor blockade. Mania has been observed in association with trazodone treatment, including in patients with bipolar disorder, as well as in patients with previous diagnoses of major depression. Compared to the reversible MAOI antidepressant drug moclobemide, significantly more impairment of vigilance occurs with trazodone.[25]
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https://en.wikipedia.org/wiki/Trazodone
Here is a throw off blog. I found from 4/17 . It's not a pubmed study but does mention a study of trazodone used with another medication to help with Alzheimer’s, Parkinson’s, and MS. This study was done on mice and is a conjecture of the findings-
https://www.psychologytoday.com/blog...in-wonder-drug
So, there's the conundrum of neuropsychopharmacology. It is far from being an exact science and can be a maze of trial and error. Especially when you mix more medications in the stew.
There are advances being made in various fields including genome and technology-
https://www.nimh.nih.gov/health/topi...nt/index.shtml
Etiology in psychiatry: embracing the reality of poly-gene-environmental causation of mental illness - Uher - 2017 - World Psychiatry - Wiley Online Library
There are additional ways of dealing with certain mental illness- psychology (CBT and ACT), nutrition, exercise, proper sleep, and certain supplements are being used and studied but I won't bog this down anymore
Hope some of this helps and you can talk to your pdoc/mental health team about all of the options! : )