Tj789
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what are the actual sciency ways that it causes addition?
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HenryHiddler
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(Original post by Tj789)
what are the actual sciency ways that it causes addition?
Okay, so the way nicotine works is that is binds to, and activates, the nicotinic acetylcholine receptors (nACh).

Long-lasting exposure to nicotine leads to both an increase in the number of these nACh receptors and a decrease in their sensitivity, leading to an overall effect of tolerance, because these desensitised receptors have to be stimulated with more nicotine for the same effect. Withdrawal occurs when the concentration of nicotine falls below the threshold needed to activate the reward pathway that is associated with nicotine (called the mesolimbic pathway AFAIK)

Hope this helps
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HenryHiddler
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(Original post by Tj789)
what are the actual sciency ways that it causes addition?
Are you in A2 biology or AS? Have you done the second messenger model in biology? The enzymes protein kinase A and protein kinase C are involved in the second messenger model - with nicotine, they phosphorylate the nACh receptor, desensitising it.

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Tj789
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(Original post by HenryHiddler)
Are you in A2 biology or AS? Have you done the second messenger model in biology? The enzymes protein kinase A and protein kinase C are involved in the second messenger model - with nicotine, they phosphorylate the nACh receptor, desensitising it.
AS- ocr, so nope
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HenryHiddler
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(Original post by Tj789)
AS- ocr, so nope
Ah okay, well, I can try to explain the basics, if you're interested - although, it isn't that important. When a substance binds to a receptor, via the second messenger model, it causes a change which activates an enzyme called adenylate cyclase, which cause ATP to turn into cAMP (cyclic AMP - just a different chemical, really). The cAMP plays the role of the second messenger, since it activates various enzymes that cause different changes (the hormone glucagon uses a second messenger, for example).

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Tj789
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(Original post by HenryHiddler)
Ah okay, well, I can try to explain the basics, if you're interested - although, it isn't that important. When a substance binds to a receptor, via the second messenger model, it causes a change which activates an enzyme called adenylate cyclase, which cause ATP to turn into cAMP (cyclic AMP - just a different chemical, really). The cAMP plays the role of the second messenger, since it activates various enzymes that cause different changes (the hormone glucagon uses a second messenger, for example).

Hope this helps
You're amazing at explaining, tanx very much!!!
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Revenged
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(Original post by HenryHiddler)
Ah okay, well, I can try to explain the basics, if you're interested - although, it isn't that important. When a substance binds to a receptor, via the second messenger model, it causes a change which activates an enzyme called adenylate cyclase, which cause ATP to turn into cAMP (cyclic AMP - just a different chemical, really). The cAMP plays the role of the second messenger, since it activates various enzymes that cause different changes (the hormone glucagon uses a second messenger, for example).

Hope this helps
This occurs with metabotropic / G protein receptors but Nicotinic AchR are ion channels / ionotropic receptors . Activation of receptor simply channel opening and this causes sodium influx.

Addiction mechanism is due to
dopamine release in reward pathways which you are correct is limbic system.

Nicotine also causes adrenal glands to release adrenaline, which has a stimulant effect via sympathetic nervous system
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HenryHiddler
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(Original post by Revenged)
This occurs with metabotropic / G protein receptors but Nicotinic AchR are ion channels / ionotropic receptors . Activation of receptor simply channel opening and this causes sodium influx.

Addiction mechanism is due to
dopamine release in reward pathways which you are correct is limbic system.

Nicotine also causes adrenal glands to release adrenaline, which has a stimulant effect via sympathetic nervous system
Thanks for the clarification. I'm aware that nicotine uses ligand-gated ion channels. I was just explaining the general mechanism behind the model, since this source says the nACh receptors are phosphorylated by the cAMP-dependent protein kinases. Are there any other mechanisms for an increase in cAMP that I'm unaware of?

Hope this helps
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Revenged
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i dont understand what has phospholyation of nicotinic AChRs got to do with nicotine addiction?

all metabotropic receptors work via intracellular mechanisms so many receptors and pathways interact simultaneously to raise and lower levels of secondary messagers, like cAMP,

tbh, it is not very well understood topic, information overload.
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HenryHiddler
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(Original post by Revenged)
i dont understand what has phospholyation [sic] of nicotinic AChRs got to do with nicotine addiction?

all metabotropic receptors work via intracellular mechanisms so many receptors and pathways interact simultaneously to raise and lower levels of secondary messagers, like cAMP,

tbh, it is not very well understood topic, information overload.
I've just realised that the point was slightly tangential - the phosphorylation would be related to desensitisation more than addiction. The withdrawal bit was more relevant. Thanks for clearing that up

Hope this helps
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