i dont understand how receptors work ,mainly the ones drugs "hit"

[HYDRO_CHRONIC]

can somone explain what results occur when hitting each receptor ,how and why does one feel sedated euphoric and what receptors are responsible with opiods, what exactly is happening

i do know that mu receptors agonists cause euphoria ,but wich receptor is responsible for sedation ,as in with methadone ,suppoosedly doesnt hit the mu receptor but still give sedation itching

dont really know how to word this ,so how many receptors are there that can cause sedation ,benzos and alcohol hit gabba,right and sedates us ,but opiods cause sedation without hitting the gabba ? and marijauna what does it hit to cause u sedation

if thgis is really vague ,my apologies ,but im bad at wording what im thinking so to speak

 

[sekio]

*All* opioid drugs, even methadone, interact with mu-opioid receptors. That's the receptor responsible for euphoria, sedation, painkilling etc. - the "good effects" of opioids.
THC from marijuana interacts at a protien cxalled the cannabinoid receptor type 1, or CB1 to produce its mental effects.
There are many other ways of producing sedation, like adrenergic antagonism (blcoking adrenaline/norepinephrine - cloinidine does this), blocking the activity of dopamine or serotonin (antipsychotics, trazodone etc), blocking the activity of histamine in the brain (diphenhydramine, chlorpheniramine etc.), GABA agonism, etc. Generally sedatives are drugs that somehow impede or block the function of one or more neurotransmitters.

Short answer: we don't really know *why* activation of e.g. mu-opioid receptor or cannabinoid receptors cause sedation/sleepiness. Other than that they perhaps inhbit your brain's signalling in some way.

Longer answer: It really depends by "hit" as some receptors can be activated in multiple ways that produce paradoxical results (for instance lisuride at 5-ht2a is an agonist but does not cause hallucinations - and LSD is an agonist that does). Some drugs also block the receptor form activating fully (partial agonists) or at all (antagonist). And there are also intricacies like splice variants and receptor dimers, where multiple receptors can "combine" to form one.

 

[HYDRO_CHRONIC]

whoa ,that just opens new questions ,i need a min ....first of all i read/heard that methadone will not cause euporia because it doesnt have the ? 3 point molecuale make up like morphine? or somthing like that

 

[sekio]

You should do more research, then. Methadone is well-known to be a mu-opioid agonist and it is for that reason it is used in pain treratment & opioid maintenance.
If you are talking about the Morphine Rule, methadone adheres to it.

Go read the Bluelight pharmacology textbook too.

Also, don't believe everything you hear about drugs, unless multiple sources back it up. Stick to sites like PubMed rather than internet forums.

 

[HYDRO_CHRONIC]

im sorry i did know it hit the mu receptor ,but was just told and read in alot of reputable peoples post that it should cause euphoria ,but yet at the right dose i feel all loveable and grin alot
dont get why stimulation of a receptor can cause euphoria,but i guess u summed it of on how restriction of chemicals etc causes the affects...

how does gbl cause euphoria and sedation and stimulation?
i just

 

[Thorns Have Roses]

GBL is a prodrug of GHB, which has excitatory effects through GHB receptor agonism, and sedative ones through GABA_B receptor agonism.

Just look up a drug on wiki and it'll give you the basic receptor targets and stuff, if that's all you wanna know.

 

[HYDRO_CHRONIC]

no im just curious as to how "the feelling" each drug gives comes to be ,like what happens in the brain ,so a receptor is stimulated ....so what whats that mean and how do we end up with the feelings we get when using drugs,alletc etc i ever hear is blah blah the receptor is stimulated THE END whats beyond the receptor,it causes this and that to happend

 

[Deleted member 170540]

no im just curious as to how "the feelling" each drug gives comes to be ,like what happens in the brain ,so a receptor is stimulated ....so what whats that mean and how do we end up with the feelings we get when using drugs,alletc etc i ever hear is blah blah the receptor is stimulated THE END whats beyond the receptor,it causes this and that to happend

Activating a receptor can open ion channels, changing the electrical potential difference between the interior and the exterior of a cell, or it can change intracellular metabolism through coupling to a 'G-protein'. Then there's steroid receptors that affect the way how genes are expressed in the cell.

All these effects change the likelyhood of the neuron 'firing' and communicating with other cells.

Neurons form very complicated networks and its almost impossible to predict what effect activating a certain class of neurons will have. Neural science hasn't advanced even near the point where one could explain what 'feelings' really are at the neuronal level.

 

[HYDRO_CHRONIC]

thank u

 

[irobeth]

*All* opioid drugs, even methadone, interact with mu-opioid receptors.

Terminology question: What about κ/δ-opioid receptors?

Is being an alkaloid a requirement for being an opioid?

 

[sekio]

Kappa/delta opioid receptors, while they do provide some facets of the "morphine experience" are not the "typical" target of opioid drugs.

And being an alkaloid is not neccesary for a drug to bind to a G-protien receptor. For instance, herkinorin (derived from salvinorin) is a potent terpenoid mu-agonist.

 

[tyrael]

....Just look up a drug on wiki and it'll give you the basic receptor targets and stuff, if that's all you wanna know.

Agree! Before any formal education this is how I built up my base-knowledge of pharmacodynamics, -kinetics, pharmacotherapies, interactions, dx and tx.

As others have said, be sure to confirm any information before committing it to memory. Especially studying off the Internet/websites...there are quite a bit of misinformation/damn flatout incorrect information out there!

....so what whats that mean and how do we end up with the feelings we get when using drugs,alletc etc i ever hear is blah blah the receptor is stimulated THE END whats beyond the receptor,it causes this and that to happend

And a reply of...

Activating a receptor can open ion channels, changing the electrical potential difference between the interior and the exterior of a cell, or it can change intracellular metabolism through coupling to a 'G-protein'....

I'm not entirely convinced the OP could understand your post*. lol


* not in respect of the accuracy or anything!

 

[irobeth]

Kappa/delta opioid receptors, while they do provide some facets of the "morphine experience" are not the "typical" target of opioid drugs.

And being an alkaloid is not neccesary for a drug to bind to a G-protien receptor. For instance, herkinorin (derived from salvinorin) is a potent terpenoid mu-agonist.

I guess what I'm asking is as with cannabinoids, since "has activity at opioid receptors" is necessary to qualify as an opioid, is it sufficient also? (I had assumed it was)

 

[MeDieViL]

GBL is a prodrug of GHB, which has excitatory effects through GHB receptor agonism, and sedative ones through GABA_B receptor agonism.

Just look up a drug on wiki and it'll give you the basic receptor targets and stuff, if that's all you wanna know.

Its more complicated, phenibut wich doesnt act on GHB is quite simular to G, stimulating and euphoric a bit, the GHB agonism further adds majorly to the euphoria.