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Cake day: July 4th, 2023

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  • The cone snail referenced in the study you linked, Conus geographus, also has the same ion channel disrupting venom that is typical of cone snails. If you were bit by one, you’d die of paralysis. It does appear to use an insulin-like peptide to initially stun the fish, but the coup de grâce is from typical paralytic conotoxins.

    A cool discovery nonetheless and TIL. Neat.

    https://pubmed.ncbi.nlm.nih.gov/25301479/

    Conus geographus is the most dangerous cone snail species known, with reported human fatality rates as high as 65%. Crude venom gland extracts have been used to determine animal LD50 and to aid the isolation of several potent paralytic toxins. […]The molecular composition of individual defense-evoked venom showed significant intraspecific variations, but a core of paralytic conotoxins including α-GI, α-GII, μ-GIIIA, ω-GVIA and ω-GVIIA was always present in large amounts, consistent with the symptomology and high fatality rate in humans.


  • deranger@sh.itjust.workstoScience Memes@mander.xyzCone snails
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    9 days ago

    I’m a former biochemist and my university studied conotoxins for use as analgesics. Cone snail venom as commonly understood are ion channel blockers. I’ve not heard of what you’re mentioning until now, but when you mention “cone snail venom”, most biology people are thinking of ion channel blockers. This is their primary method of disabling prey.

    If you’re bit by a cone snail and try to drink some soda to counteract the toxin, you’re going to have a bad time. They’re called cigarette snails because you’ve got time to smoke one cig before you die - and not from low blood sugar.

    From your source:

    For example, fish-hunting cone snails use a “motor cabal” to disrupt the propagation of action potentials at the neuromuscular junction. Motor cabal toxins include those that block presynaptic voltage-gated calcium channels (CaV), postsynaptic nicotinic acetylcholine receptors (nAChR), and voltage-gated sodium channels (NaV) on muscle cells6.

    From Wikipedia:

    https://en.wikipedia.org/wiki/Conotoxin

    As of 2005, five biologically active conotoxins have been identified. Each of the five conotoxins attacks a different target:
















  • You’re not comprehending what you’re reading. In that sentence, when it says it modulates the pro-inflammatory and anti-inflammatory response, it’s saying it affects both, It’s not saying that the nervous system itself is pro-inflammatory.

    Together, these results uncovered two lines of signalling from the vagal ganglia to the brain. One line (TRPA1) carries anti-inflammatory signals and acts on cNST neurons to enhance the anti-inflammatory response (for example, by positive feedback onto immune cells releasing anti-inflammatory cytokines) and helps to suppress the pro-inflammatory state. The other (CALCA neurons) responds to pro-inflammatory signals and helps to tune down the pro-inflammatory response (for example, by negative feedback onto immune cells releasing pro-inflammatory cytokines).

    To “tune down a pro-inflammatory response” and “enhance an anti-inflammatory response” are both anti-inflammatory effects achieved through modulating both anti- and pro- inflammatory responses. Enhance one, diminish another.


  • deranger@sh.itjust.workstoScience Memes@mander.xyzI've got a fever...
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    1 month ago

    We demonstrate that pro-inflammatory and anti-inflammatory cytokines communicate with distinct populations of vagal neurons to inform the brain of an emerging inflammatory response.

    Where do you think those cytokines that are influencing the nervous system come from? White blood cells. That’s where it all starts, not the nervous system. You’re putting the cart before the horse.

    Chemogenetic activation of the cNST neurons during an immune response suppresses inflammation.

    The study you linked demonstrates the brain suppresses inflammation/fever, not promotes it.