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It is known that various chemicals can bind to the same receptor type, producing different effects. Be these chemicals agonists or antagonists, there are more variations in how they influence the receptor than just sending an activation or inhibition signal. There seem to be various flavours of activation (not sure about inhibition), where, for example, a psychedelic drug binding to a serotonin receptor produces a different result than serotonin itself.

For a more clear representation, I have split the question into logical parts:

  1. What is the essense of this difference? Does it come from the chemicals molecule properties like shape and electron configurations of the atoms?

  2. If we were to draw two comparative pictures of how two such different chemicals affect a receptor, how would we picture that? What would we chose to be the characteristic figure(s) on our pictures? What qualities of the connection (probably changing over time) would we consider to display on the picture?

Does this question make sense or are there any false assumptions?

UPDATE:

Response to the comment by WYSIWYG: I cannot cite any source saying so. It is that I got this question at some point: is ligand-receptor activation a binary function, which can only give either 0 (no interaction or inhibition) or 1 (activation) values, or it is something more varied?

Taking into account that ligand-receptor interaction is molecule-molecule, it is logical to assume that the resulting complex can put the receptor molecule in a variety of states, depending on the ligand molecule structure. Here the Ionic Bonds and Hydrogen Bonds sections shed some light on this - the described interaction patterns seem like they can produce quite different results. Like, for example, they put receptors molecules electron cloud configurations in different states. But does in reality such interaction always result in either 0 or 1 state of the receptor?

The pdf paper refered from this question leaves the reader to guess: are the varying effects of the chemicals produced solely by their profile of different affinity to different groups of receptors, or do they also interact with each receptor type differently. In other words, is the drug effect produced by a certain amount of 1s being fired by the receptors, or is it changing the quality of their firing signal itself, i.e. making the receptor to initiate different, non-typical processes inside the cells?

Or, in the cited Wikipedia article, under section The specificity of drugs it is said that muscarine and nicotine can selectively activate specific subtypes of acetylcholine receptors. Is the result of these chemicals activating these receptors exactly the same as of acetylcholine? If we deliver both muscarine and nicotine to their sites, will they produce the same effect as if we deliver acetylcholine to both of them?

Also, I cannot really find much information on what lies beyond the receptor, namely - how does it send the signal somewhere else.. but I guess that's molecule-molecule again, so here we get the chance of varying result too. Or don't we?

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    $\begingroup$ Agonists primarily act by mimicking the actual ligand (molecular homology). They basically elicit the same effect as the actual molecule. Can you cite an example where two ligands binding to the same receptor elicit different responses. This seems theoretically possible depending on the signalling network downstream of the receptor. $\endgroup$ – WYSIWYG Sep 17 '15 at 18:18
  • $\begingroup$ @WYSIWYG: I have replied to your question in the update to the original question. $\endgroup$ – noncom Sep 17 '15 at 21:43
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    $\begingroup$ Search term you are looking for is "promiscuous". GPCR are very promiscuous. Look at these articles 1, 2, 3, 4. Similary you will find many explaining this common phenomenon. $\endgroup$ – Dexter Sep 18 '15 at 4:04

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