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bicbrownboi t1_j5ix3ue wrote

Turnover rate is relevant for neurotransmitters which are degraded within the synapse. Some NTs are not (see serotonin- not degraded within the synapse to a significant degree, mostly reuptaken by the presynaptic side). Acetylcholine on the other hand is degraded by acetylcholinesterase within the synapse, and its components are then reuptaken. Turnover rate refers to the degradation rate (basically the amount of acetylcholinesterase in the synapse)

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Citrownklown t1_j5j2wpc wrote

Replying to bicbrownboi (#1,448,522)

Good point.

AcCh turnover increase means more is degraded by the enzyme, decrease the opposite.

Depending on the location of the turnover (central nervous system or e.g. In skeletal muscles) this could lead to prolonged or shorter duration of AcCh.

One cool example of a drug working by decreasing AcCh effect (ultimately) is botox, leading to temperary paralysis on the injection site.

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Quiz_Quizzical-Test_ t1_j5jeza3 wrote

Bic answered the first half of your question. I don’t know what lens you are coming at this from, so I’ll dump a little bit of medical and biochem in the answer.

As for the second half, if turnover rate goes down, neurotransmitter duration of action is increased. One such drug class that has that action are cholinesterase inhibitors (-stigmines). Their action increases the synaptic half life of acetylcholine by inhibiting acetylcholinesterase, and that manifests as increased cholinergic activity (SLUDGEM or DUMBBELLS are two menonics you can look up if you’d like). Stigmines are reversible and competitive (until they aren’t…they eventually can “mature” into irreversible) so they only impact Vmax, not Km.

Anti-cholinergics do the opposite action at those synapses. They bind the ACh receptor without producing an effect increasing accessibility of ACh to acetylcholinesterase. I can’t comment to what degree this effect increases the turnover of ACh. The Km of acetylcholinesterase from a quick google is somewhere in the realm of 10 mM making me think it does not operate in a saturated fashion, but it’s been a decade since I’ve learned this stuff. It seems increasing substrate supply would increase rate too.

Hope this helps.

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daywalkker t1_j5jkb6v wrote

Replying to Devil_May_Kare (#1,448,587)

Not just Sarin, any organophosphate can hamper the ACh turnover rate. Remember the signs of organophosphate toxicity: SLUDGE

Salivation

Lacrimation

Urination

Defecation

Gastroenteric problems

Emesis

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Thugluvdoc t1_j5jpqfg wrote

Think of neurotransmitters (NT) as a person, and the synapse/neuron as a button. Imagine there are a group of people whose job is to press the buttons (stimulate the neurons) as many times and as often as possible but they get tired and leave. So turnover rate means how often the person gets tired and leaves the button alone. SSRIs do not allow serotonin to be “reuptaken” or in this example, the person in the room pushing buttons isn’t allowed to leave so he’s constantly pushing the buttons (stimulating the receptor). That’s a basic overview. Obviously overstimulation means your body down regulates the receptor (less buttons to push), and the opposite happens when you take something away from the body - your body upregulates the receptor - puts more buttons hoping to find a neurotransmitter (person) to stimulate it (push the button). Sorry if this sucks, hope it helps.

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BirdLawyerPerson t1_j5jqppg wrote

Replying to Bax_Cadarn (#1,450,557)

Any acronym related to illness, disease, or medical issues, I just assume come from medical students trying to cram for exams. The sheer amount of lists they have to memorize makes acronyms a pretty good memorization technique.

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nervouscomposure t1_j5jy9oq wrote

Replying to Quiz_Quizzical-Test_ (#1,449,968)

Very interesting, thanks for the pharmaceutical explanation. I take a cholinergic drug to treat Myasthenia Gravis, a disease caused directly by acetylcholine binding issues, so my ears perk up anytime I see the little molecule mentioned. For me, the decreased turnover means better voluntary muscle function

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Citrownklown t1_j5kdjzt wrote

Replying to curiousnboredd (#1,452,576)

It looks like the mode of action of botox is a bit more complex (here’s from one of my favorite webpages drugs@fda)

12.1 Mechanism of Action BOTOX blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. When injected intramuscularly at therapeutic doses, BOTOX produces partial chemical denervation of the muscle resulting in a localized reduction in muscle activity. In addition, the muscle may atrophy, axonal sprouting may occur, and extrajunctional acetylcholine receptors may develop. There is evidence that reinnervation of the muscle may occur, thus slowly reversing muscle denervation produced by BOTOX.

https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/103000s5236lbl.pdf#page13

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