Well, most drugs tend to be either agonists, or antagonists, or different variations thereof, there are many different flavors of agonists and antagonists, such as partial and full agonism, inverse agonism vs antagonism, etc.
With opioids, the most commonly abused, most euphoric drugs tend to be the full agonists: Morphine, Heroin, Hydro/OxyCodone, Hydro/OxyMorphone, Methadone.
When someone is overdosing on a full agonist due to excessive CNS depression, they are administered with the opioid antagonist, naloxone (Narcan). Naloxone rips the full agonist off the opioid receptors because it has a much stronger binding affinity for the opioid receptors than the full agonist the person was overdosing on. Antagonists work in the opposite way of the agonist.
With benzodiazepines, most are full agonists on the GABAergic receptors, and in situations where benzodiazepines are part of suspected overdose, they are administered with flumazenil, a benzodiazepine antagonist, which reverses the benzodiazepine aspect of the overdose and a lot of the CNS depression is lifted.
Because they are opposites, just like how most benzodiazepine
agonists have anti-convulsant properties, and protect against seizures, if one were to administer too much of a benzodiazepine
antagonist, such as flumazenil, it will act as a convulsant and induce seizures.
Anyways back to the opioids, suboxone = buprenorphine / naloxone. Both of these drugs have an extremely high binding affinity for the opioid receptors, buprenorphine's binding affinity is even higher than naloxones, which is what discredits the claims made by pharmaceutical company that marketed Suboxone, they said it would be hard to abuse due to the naloxone content, but this was rapidly disproven as many addicts proceeded to inject Suboxone tablets anyways, without inducing the precipitated withdrawals the pharmaceutical company claimed they would, so the whole abuse-proof aspect of Suboxone is bullshit.
Buprenorphine, the active ingredient in Suboxone, is a partial opioid agonist. At low doses, it acts as a potent opioid agonist, which can produce euphoric sensations almost like the full agonists (morphine, oxycodone, hydromorphone, etc) but buprenorphine has a ceiling effect. It's a partial agonist because at low doses, it behaves as a full agonist, but at higher doses, like 2mg and up, it begins to naturally antagonize itself and other opioids, producing a blockade effect where you reach a limit, reducing the ability to feel euphoria. During the induction phase of Suboxone maintenance, doctors may prescribe 24-32mg per day, even though many studies have shown that there is no therapeutic benefit to dosing higher, most people will be just fine on less than 8mg per day.
Buprenorphine is extremely potent and raises the users tolerance very quickly and has a very long half life, making it a good candidate for a maintenance drug, however due to it being a partial agonist (behaving like an agonist at low doses, and an antagonist at higher doses), it's not like methadone, which is a full agonist where you can raise the dose indefinitely if need be.
It is very uncommon for patients to need more than 8mg per day, and the lower the dose of Suboxone you can get down to, the better...
Make any sense?
edit:
http://issues05.emcdda.europa.eu/en/page032-en.html
Source: Adapted from Jones, H. E. (2004), 'Practical considerations for the clinical use of buprenorphine', Science & Practice Perspectives 2, no. 2, pp. 4-20.
