When this key (antagonist) is inserted in the lock, the proper key (agonist) can’t go into the same lock. The main active ingredient in cannabis, THC, is an agonist of the cannabinoid receptor, and hallucinogenic drug LSD is a synthetic molecule mimicking the agonist actions of the neurotransmitter serotonin at one of its many receptors – the 5HT2A receptor.Īn antagonist is a drug designed to directly oppose the actions of an agonist.Īgain, using the lock and key analogy, an antagonist is like a key that fits nicely into the lock but doesn’t have the right shape to turn the lock. Specific effects such as pain relief or euphoria happen because opioid receptors are only present in some parts of the brain and body that affect those functions. By luck it mimics the shape of the natural opioid agonists, the endorphins, that are natural pain relievers responsible for the “endorphin high”. Morphine, for instance, wasn’t designed by the body but can be found naturally in opium poppies. The natural agonist is the master key but it is possible to design other keys (agonist drugs) that do the same job. Simply put, an agonist is like the key that fits in the lock (the receptor) and turns it to open the door (or send a biochemical or electrical signal to exert an effect). Many drugs are made to mimic natural agonists so they can bind to their receptors and elicit the same – or much stronger – reaction. But morphine – or heroin that turns into morphine in the body – is an artificial agonist of the main opioid receptor.Īn artificial agonist is so structurally similar to a receptor’s natural agonist that it can have the same effect on the receptor.
They can be natural or artificial.įor instance, endorphins are natural agonists of opioid receptors. An agonist is something that causes a specific physiological response in the cell. Those molecules that bind to specific receptors and cause a process in the cell to become more active are called agonists. This signal then makes the cell do certain things such as making us feel pain. Opioid receptors have many other and more important roles in the brain and periphery however, modulating pain, cardiac, gastric and vascular function as well as possibly panic and satiation, and receptors are often found at postsynaptic locations as well as presynaptically.These outside molecules bind to receptors on the cell, activating the receptor and generating a biochemical or electric signal inside the cell. By hijacking this process, exogenous opioids cause inappropriate dopamine release, and lead to aberrant synaptic plasticity, which causes dependency. In the classical sense, μ opioid receptors are presynaptic, and inhibit neurotransmitter release through this mechanism, they inhibit the release of the inhibitory neurotransmitter GABA, and disinhibit the dopamine pathways, causing more dopamine to be released. μ-Opioid receptors are the main receptor through which morphine acts.
Β-Endorphin has the highest affinity for the μ 1 opioid receptor, slightly lower affinity for the μ 2 and δ opioid receptors, and low affinity for the κ 1 opioid receptors.
In situations where the level of ACTH is increased (e.g., Cushing’s Syndrome), the level of endorphins also increases slightly. The behavioural effects of β-endorphin are exerted by its actions in the brain and spinal cord, and it is presumed that the hypothalamic neurons are the major source of β-endorphin at these sites. β-Endorphin is a cleavage product of pro-opiomelanocortin (POMC), which is also the precursor hormone for adrenocorticotrophic hormone (ACTH). The β-endorphin that is released into the blood cannot enter the brain in large quantities because of the blood–brain barrier, so the physiological importance of the β-endorphin that can be measured in the blood is far from clear. Beta-endorphin (β-Endorphin) is released into blood from the pituitary gland and into the spinal cord and brain from hypothalamic neurons.