As mentioned above, agonists have the potential to bind in different locations and in different ways depending on the type of agonist and the type of receptor. The process of binding is unique to the receptor-agonist relationship, but binding induces a conformational change and activates the receptor. This conformational change is often the result of small changes in charge or changes in protein folding when the agonist is bound. Two examples that demonstrate this process are the muscarinic acetylcholine receptor and NMDA receptor and their respective agonists.
For the muscarinic acetylcholine receptor, which is a G protein-coupled receptor(GPCR), the endogenous agonist is acetylcholine. The binding of this neurotransmitter causes the conformational changes that propagate a signal into the cell. The conformational changes are the primary effect of the agonist, and are related to the agonist's binding affinity and agonist efficacy. Other agonists that bind to this receptor will fall under one of the different categories of agonist mentioned above based on their specific binding affinity and efficacy.
The NMDA receptor is an example of an alternate mechanism of action, as the NMDA receptor requires co-agonists for activation. Rather than simply requiring a single specific agonist, the NMDA receptor requires both the endogenous agonists, N-methyl-D-aspartate (NMDA) and glycine. These co-agonists are both required to induce the conformational change needed for the NMDA receptor to allow flow through the ion channel, in this case calcium. An aspect demonstrated by the NMDA receptor is that the mechanism or response of agonists can be blocked by a variety of chemical and biological factors. NMDA receptors specifically are blocked by a magnesium ion unless the cell is also experiencing depolarization.
These differences show that agonists have unique mechanisms of action depending on the receptor activated and the response needed. The goal and process remains generally consistent however, with the primary mechanism of action requiring the binding of the agonist and the subsequent changes in conformation to cause the desired response at the receptor. This response as discussed above can vary from allowing flow of ions to activating a GPCR and transmitting a signal into the cell.