Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012


What are the three main NTs implicated in depression?



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What is the neuroscience behind depression?
What are the three main NTs implicated in depression?
What seems to be the case for each of them?

    • Norepi

      • MAO also breaks down norepinephrine. MAO inhibitors treat depression.

      • Reserpine degrades norepi vescicles and can trigger depression.

      • Post-mortem examination of brains from depressed people show lower levels of norepi than normal.

      • So it seems like it's a problem of too little norepinephrine. Tied to the psychomotor retardation symptom.

      • BUT: MAO inhibitors work molecularly within hours but they don't improve depression for weeks. So it may have to do with autoregulation and even opens up the possibility that it's too much norepi.

    • Serotonin

      • Prozac and other selective serotonin reuptake inhibitors have the same issues with time-course as norepi and MAO inhibitors.

      • Tied to the rumination/perseveration symptoms.

    • Dopamine

      • Central to pleasure, so maybe has to do with this anhedonia sympsoms.
But then what other neurochemicals are implicated in depression and in what way?

    • Substance p has to do with pain pathways, a possible link to psychic pain

    • Inflammation triggers sickness behavior which is really similar to psychomotor retardation and lowered mood.

    • CRH neurons project to midbrain structures and brainstem nuclei that activate the sympathetic NS. That's where the stress part comes from.

    • BDNF is abnormal in depression too: important for neurogenesis and neural complexity.




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