When Grasshoppers Go Biblical: Serotonin Causes Locusts To Swarm

Discussion in 'Articles & Scientific Studies' started by Dessert_All_Day, Nov 20, 2018.

  1. Terma

    Terma Member

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    You could run this experiment: You starve control mice and mice administered p-chrolo-whatever-the-TH-inhibitor-is-again, and you record their activity until they die (Auschwitz for mice... is this evil yet?). The p-chloro mice would die faster (while having more fight in them), but you should still be able to deduce something from their progression...
     
  2. Terma

    Terma Member

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    To clarify, the way I imagine this, is that the SERT-inhibition-triggered buildup may be just the first in one or more food restriction adaption responses that promote increased activity... Because both for locusts swarming and that caloric restriction study, the circumstances don't seem to me to be that extreme. So perhaps past a second point in starvation, something else promotes increased activity?

    Here's one of several possible mechanisms:
    Kynurenic acid is a nutritional cue that enables behavioral plasticity

    Since kynurenine pathway modulates feeding in lower organisms, there could be something similar or derived in higher-level organisms. I figure maybe serotonin is an extra adaptation to the threat of scarcity on top of the kynurenine pathway, for survival of higher organisms? But they may still work in tandem.

    So if you remove serotonergic influence, you're still left with the possibility of lowered kynurenic acid and increased quinolinic acid (the latter only to some extent or possibly caused by B vitamin deficiency?), which should trigger increased desperation and food search...

    So I wonder in parallel, past a further point of deprivation, what exactly happens to serotonin, compared to kynurenine (or other signal)...

    (Also note in that study the "neuropeptide-y-like" pathways (due to low KYNA), not sure how conserved that is in mammals - I still have to read more, always more, and more - but that is possibly a crucial link)
     
  3. Terma

    Terma Member

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    And that brings up another point, which is that the Kynurenine pathway (via TDO) has been thought to account for much more Tryptophan consumption than the serotonin pathways... in part to go toward NAD production... So what if the tissue breakdown Trp all goes toward Kyn/NAD? [Or is it tissue-local enough to bypass this issue?]

    [Edit: Yet another complication: a major TDO inducer in the liver is cortisol, which is clearly going to be high and can only get lower if hormone synthesis dies off - but I don't currently know what happens to that induction if the glucocorticoid receptors becomes insensitive vs sensitive, assuming it does for that - it's probably described somewhere...]