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Cognitive versus well-being enhancement?

Neuroprotection said:
Exactly, I agree with you. lithium definitely seems to kill emotion both negative and positive but I think it’s slightly stronger in suppressing positive emotions, and that’s why it is deemed highly useful for treating bipolar mania. not saying lithium doesn’t help, it has probably saved many lives, but having no emotion seems just awful and I’m not surprised people have referred to lithium and antipsychotics as evil medications. in my opinion, self-medication is sometimes really underrated, of course, so long as it’s not something that’s detrimental or unsustainable. I read a lot about how my favourite drug nicotine supposedly doesn’t help with stress and with regular use, makes anxiety and procrastination worse. strangely, whenever I managed to get hold of very high nicotine Vapes or chewing tobacco and used it daily over a few months I became much more happy and resilient and I procrastinated much less. Yes, it’s true there was no direct cognitive enhancement as my memory didn’t improve, but nicotine somehow stabilise my mood whilst lifting it slightly and not affecting my natural emotional responses. when I tell people about this, nobody believes me and they say self-medication, which doesn’t work. I guess I can never prove to them that it does, unless they could somehow see into my conscience!
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The medicinal benefits of lithium are perfect for some people who have been in an ongoing struggle with bipolar disorders and I can definitely see why they would want to keep from getting overly happy and/or sad! However, although I’m absolutely not a physician if you are able to lead a relatively healthy lifestyle with minimal risk of your mood disorder being a problem then I would just ride it out. Like I said, just how I feel personally I’m absolutely no doctor haha
 
Neuroprotection said:
I think there’s something similar going on for those who think nicotine/tobacco is a cognitive enhancer. yes, it does boost cognition at low doses in those without tolerance, but it’s a very minor/Insignificant effect which likely dissipates completely at higher doses and never returns after tolerance. The real benefits of nicotine, especially from cigarettes or chewing tobacco, comes from the induction of dopamine release and the sense of calm it brings to one having to carry out depressing/boring tasks.

What do you all think?
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I thought it was due to nicotine raising CaMKII activity to help with LTP, at least a significant portion of the memory enhancing benefit
 
stayUpallN1ght said:
Could you explain what CaMKII activity is? As well as LTP? I’m curious to know how it works.
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Long-term potentiation(LTP) is the strengthening of synapses, usually by the creation and insertion of new neurotransmitter receptors such as glutamate AMPA receptors into the postsynaptic membrane. The other two forms of LTP I know of are enhance neurotransmitter release from the presynaptic neuron or modification of already existing postsynaptic neurotransmitter receptors to make them more sensitive to neurotransmitters. basically, LTP enhances the efficiency and strength of connection between two neurons and it’s thought to be the basis of learning and memory. regarding CaMKII, that is a calcium-dependent enzyme that stimulates LTP by attaching a phosphate group to already existing AMPA glutamate receptors and if I’m not mistaken, that makes them much more sensitive to glutamate. since AMPA receptors are vital for memory encoding, stimulating this enzyme could theoretically improve memory. however, I doubt chronic nicotine would continuously activate it and that’s a good thing because excessive or uncontrolled LTP is believed to be at the core of epilepsy onset, maintenance and exacerbation.
 
CaMKII is a proteins assembly that does a while bunch of shit. One of those shits is phosphorylating proteins that are involved in getting more AMPA and NMDA receptors into the synapse to make response to glutamate for efficient strengthening the connection between those two neurons

That is a large mechanism behind Long Term Potentiation, there are a whole bunch of other mechanisms as well such as swapping out AMPA and NMDA receptor subunits and phosphorylating them to modify their conductance, open probability, and kinetics to the same end of increasing responsiveness of the receiving neuron

There are also mechanisms of the reverse call Long Term Depression but that's a whole 'nother story that I'm not as familiar with but both of these concepts underlie memory

Here's a nice picture showing come CaMKII pathway stuff related to LTP

Other pathway stuff


And here are some papers as well from which the images came, in order
www.ncbi.nlm.nih.gov

Mechanisms of CaMKII action in long-term potentiation

Long-term potentiation (LTP) of synaptic strength occurs during learning and can last for long periods, making it a probable mechanism for memory storage. LTP induction results in calcium entry, which activates calcium–calmodulin-dependent protein ...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov


www.frontiersin.org

CaMKII in sinoatrial node physiology and dysfunction

The calcium and calmodulin-dependent protein kinase II (CaMKII) is present in sinoatrial node (SAN) pacemaker cells and is required for physiological “fight or flight” SAN beating rate responses. Inhibition of CaMKII in SAN does not affect baseline heart rate, but reduces heart rate increases in...
www.frontiersin.org www.frontiersin.org
 
Neuroprotection said:
Long-term potentiation(LTP) is the strengthening of synapses, usually by the creation and insertion of new neurotransmitter receptors such as glutamate AMPA receptors into the postsynaptic membrane. The other two forms of LTP I know of are enhance neurotransmitter release from the presynaptic neuron or modification of already existing postsynaptic neurotransmitter receptors to make them more sensitive to neurotransmitters. basically, LTP enhances the efficiency and strength of connection between two neurons and it’s thought to be the basis of learning and memory. regarding CaMKII, that is a calcium-dependent enzyme that stimulates LTP by attaching a phosphate group to already existing AMPA glutamate receptors and if I’m not mistaken, that makes them much more sensitive to glutamate. since AMPA receptors are vital for memory encoding, stimulating this enzyme could theoretically improve memory. however, I doubt chronic nicotine would continuously activate it and that’s a good thing because excessive or uncontrolled LTP is believed to be at the core of epilepsy onset, maintenance and exacerbation.
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Oh wow that’s awesome! I appreciate you taking the time to share that information! Thank you!
 
stayUpallN1ght said:
Oh wow that’s awesome! I appreciate you taking the time to share that information! Thank you!
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You’re very welcome. I love sharing The little scientific knowledge I have gathered. Can’t say I understand neuroscience that well but I love learning about neuroscience concepts, especially as they relate to emotion and to try and apply this to daily life or at least understand why we feel the way we do.
 
in regards to the growing use of smart drugs(Mental performance enhancers) I think researchers should focus more on how these drugs actually help people without being judgemental. i’ve heard criticism from professionals Who say things like; Smart drugs, don’t actually make you smarter but just help you focus, or that they simply help you stay awake. The question then becomes, if it helps people get the job done what’s wrong with that? then there’s the very relevant and direct attack on traditional amphetamine type psychostimulants. this is the argument that such stimulants have little to no cognitive benefits in healthy people. in fact, they might be the least helpful of all drugs in this regard, but instead they work by creating a powerful sense of drive and motivation by elevating dopamine levels. elevated dopamine also makes hi effort/very boring tasks which generally make up most of the workday, feel much easier and much less boring. just a disclaimer, I know psychostimulants have serious side-effects and until safer analogues or protective countermeasures, based on in-depth neuroscience understanding are created, I don’t believe everyone should use them. back to the argument that Psychostimulants just make tasks less boring, my argument remains the same. If it helps people then what’s wrong with it? as long as people are informed, I think they should be able to make their own choices.
 
although I’ve never tried drugs/stimulants beyond caffeine and nicotine, i’ve learned from experience that procrastination in itself will almost never be treated instantaneously with a drug even if you have ADHD. from reflecting on my own experiences of studying/working over the past few months, I found that my procrastination is probably due to deep internalised fear/trauma from the constant heavy threat of serious consequences from procrastinating hanging over my head since childhood and the stress of last-minute deadlines.
Nicotine, which has in the past really helped me as has caffeine, only did so when I took them regularly and when I was already disciplined and in the right frame of mind to be working on the dreaded task at hand. At that point, those drugs would provide energy which of course help me focus, but more importantly, a sense of optimism about the good results of getting the task done including getting it out of the way.
 
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