Receptor signalling is dependent on agonist and antagonist binding. On the binding of an agonist, the receptor undergoes a conformational change allowing it to catalyse a reaction within the cell, releasing a second messenger molecule and activating a signalling pathway.
Agonists activate receptors, with endogenous agonists being found naturally in cells. Synthetic, exogenous agonists, can also be used to activate signalling pathways – such as with drugs. A notable example is opioids, acting as a partial agonist on the opioid receptor – this can be exploited for euphoric and analgesic effects.
Antagonists inhibit the activation of receptors. This is exploited by drugs, suppressing signalling pathways.
Agonists bind to the allosteric site, allowing them to have their activating effect. Antagonists can bind to either the allosteric or the orthosteric site, either blocking the agonist binding site or changing the structure sufficiently that it is no longer able to be bound by the endogenous agonist.
Benzodiazepines modulate the activity of the GABA_A receptor, increasing the excitability of inhibitory neurotransmission. As a positive allosteric modulator, it does not interact with the orthosteric site, allowing GABA to activate the receptor as it would normally. Benzodiazepines do not activate the receptor – it is only made more excitable.