Thanks for the video!!! Some questions, how does the Adenosine that builds up when the receptors are full not get reuptaken by the pre-synaptic neuron or broken down by enzymes? Also, when you drink caffeine, does it start to decrease the sensitivity of your neurons like Nicotine does by adding more receptors?
I am an avid #MentalHealthAwareness advocate and performer, and I love this so much. I travel the country trying to bring that awareness on stages, in classrooms, hospitals, and on my TH-cam channel, so I get excited when I see other advocates. 💙❤
Is it possible to manipulate the crash to have an easier time falling asleep? What I am getting at is: What if I drink coffee 8 hours before I am going to bed, and then the crash comes right as I want to sleep. Btw, your videos are very useful, I appreciate the effort!
I'm glad you're finding the videos useful! As for scheduling, unfortunately the crash and complete elimination of caffeine don't occur at the same time. The crash would probably occur a few hours after consumption, though some caffeine would remain in your body much longer. The most noticeable effects usually wear off after about 4-6 hours, which is about the half-life of caffeine in the body (though people vary in how efficiently they can break down caffeine). This means half of the caffeine consumed would still be present 4-6 hours later, and this would likely disrupt the quality of your sleep. By 8 hours most caffeine would likely be eliminated, but the crash would have occurred a few hours before that. Hope this helps!
Hi there! Firstly, I want to thank you on your really succinct and informative explanations, they have helped me a lot! However, i hope that you'll be able to explain to me on the part where you talked about the caffeine and adenosine NT. I remember in one of your videos you spoke about the autoreceptors on the presynaptic membrane which monitor the level of NT of the synaptic cleft and that it would inhibit the release of more NT if the level gets too high. So by applying that info, i can't seem to understand why the the axon terminals of the presynaptic membrane continue to release adenosine.. Also, is the adaptation you spoke of related to neuroplasticity?
Great question about adenosine! I probably should have clarified that adenosine is a neurotransmitter but it doesn't function like most classic examples of neurotransmitters. Adenosine isn't released from vesicles and this is why the level continues rising around cells despite a high concentration. For more details on adenosine this first article from the Encyclopedia of Neuroscience might be helpful: www.sciencedirect.com/topics/agricultural-and-biological-sciences/adenosine The neuroadaptation that I talked about for drugs is more focused on micro-level changes in things like chemical signaling, while neuroplasticity usually refers more to broader changes in the functioning or structure of brain regions but these two concepts are certainly related and neuroadaptation may lead to broader functional changes over the long-term.
TrashKnight We can generally use the analogy of a neurotransmitter and receptor working like a lock (the receptor) and key (the neurotransmitter). In this case the nicotine molecule has a similar enough structure to the acetylcholine molecule that it can also fit like a key in the ACh receptor.
Thanks! Really helpful :D. But one last question, can you explain how stimulation of central nAChRs by nicotine results in the release of a variety of neurotransmitters in the brain?
I can try :) The general idea is that acetylcholine receptors are also found on neurons that release other neurotransmitters. This means that the presence of nicotine changes the excitability of these neurons and thus influences the release of their neurotransmitters. One area where this occurs is in the ventral tegmental area of the midbrain where nicotine influences activity of both GABA and dopamine neurons. This activity is associated with feelings of pleasure and reward and relates to the addictive nature of nicotine. You can read some of the finer details of this process here: www.researchgate.net/publication/9004423_Cholinergic_modulation_of_dopaminergic_reward_areas_Upstream_and_downstream_targets_of_nicotine_addiction
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Again, a beautiful explanation, blown away at the Nicotine example. You're a very good teacher.
Thanks!
wow this video is really good! You explained this better than my masters lecturer at a top university! I instantly understood what you meant.
That's great to hear, I'm glad I could help!
Freaking useful, why does this have only 935 views?
Really clear and easy to understand. Thank you!
You're welcome!
Wow. Simply delivered😘😘
Thanks for the video!!! Some questions, how does the Adenosine that builds up when the receptors are full not get reuptaken by the pre-synaptic neuron or broken down by enzymes? Also, when you drink caffeine, does it start to decrease the sensitivity of your neurons like Nicotine does by adding more receptors?
You just made this so much easier for me. Thank you!
Thanks, that's why I make these videos so I'm really glad to hear that!
This is an awesome explanation!
Thank you so much for explaining it in such a clear and simple way
You're welcome!
I am an avid #MentalHealthAwareness advocate and performer, and I love this so much. I travel the country trying to bring that awareness on stages, in classrooms, hospitals, and on my TH-cam channel, so I get excited when I see other advocates. 💙❤
The caffeine example is awwwwesome😂
Thank you!! Just a tiny remark at 6:00 - Adenosine is not a neurotransmitter, but a neuromodulator.
You're right that in this case adenosine is functioning as a neuromodulator so using that term would have been more precise. Thanks for commenting!
Wow. You explained this really well.
Thanks, hope it was helpful!
Is it possible to manipulate the crash to have an easier time falling asleep? What I am getting at is: What if I drink coffee 8 hours before I am going to bed, and then the crash comes right as I want to sleep. Btw, your videos are very useful, I appreciate the effort!
I'm glad you're finding the videos useful! As for scheduling, unfortunately the crash and complete elimination of caffeine don't occur at the same time. The crash would probably occur a few hours after consumption, though some caffeine would remain in your body much longer. The most noticeable effects usually wear off after about 4-6 hours, which is about the half-life of caffeine in the body (though people vary in how efficiently they can break down caffeine). This means half of the caffeine consumed would still be present 4-6 hours later, and this would likely disrupt the quality of your sleep. By 8 hours most caffeine would likely be eliminated, but the crash would have occurred a few hours before that. Hope this helps!
Wow! Amazing presentation!
Thanks!
Great video and explanation.
Thanks!
Thank you sir.......
You are fantastic !
Marcos Vinicius Thanks!
Hi there! Firstly, I want to thank you on your really succinct and informative explanations, they have helped me a lot!
However, i hope that you'll be able to explain to me on the part where you talked about the caffeine and adenosine NT. I remember in one of your videos you spoke about the autoreceptors on the presynaptic membrane which monitor the level of NT of the synaptic cleft and that it would inhibit the release of more NT if the level gets too high. So by applying that info, i can't seem to understand why the the axon terminals of the presynaptic membrane continue to release adenosine..
Also, is the adaptation you spoke of related to neuroplasticity?
Great question about adenosine! I probably should have clarified that adenosine is a neurotransmitter but it doesn't function like most classic examples of neurotransmitters. Adenosine isn't released from vesicles and this is why the level continues rising around cells despite a high concentration. For more details on adenosine this first article from the Encyclopedia of Neuroscience might be helpful: www.sciencedirect.com/topics/agricultural-and-biological-sciences/adenosine
The neuroadaptation that I talked about for drugs is more focused on micro-level changes in things like chemical signaling, while neuroplasticity usually refers more to broader changes in the functioning or structure of brain regions but these two concepts are certainly related and neuroadaptation may lead to broader functional changes over the long-term.
@@PsychExamReview thank you for your reply and clarification!! ☺️☺️ I really appreciate your videos!!
this is so good!!!!..thanks a lot!!!
You're welcome!
you are the best
😀😀
Thanks!
How can nicotine bind with the acetycholine receptors?
TrashKnight We can generally use the analogy of a neurotransmitter and receptor working like a lock (the receptor) and key (the neurotransmitter). In this case the nicotine molecule has a similar enough structure to the acetylcholine molecule that it can also fit like a key in the ACh receptor.
Thanks! Really helpful :D. But one last question, can you explain how stimulation of central nAChRs by nicotine results in the release of a variety of neurotransmitters in the brain?
I can try :) The general idea is that acetylcholine receptors are also found on neurons that release other neurotransmitters. This means that the presence of nicotine changes the excitability of these neurons and thus influences the release of their neurotransmitters. One area where this occurs is in the ventral tegmental area of the midbrain where nicotine influences activity of both GABA and dopamine neurons. This activity is associated with feelings of pleasure and reward and relates to the addictive nature of nicotine. You can read some of the finer details of this process here:
www.researchgate.net/publication/9004423_Cholinergic_modulation_of_dopaminergic_reward_areas_Upstream_and_downstream_targets_of_nicotine_addiction
I can drink a huge coffee just before bed and still fall asleep in 30 seconds
Wow I owe you my life 😂