Hyperthesis
Bluelighter
+1 for Sekio's short summary of basic pharmacology terms.
I would still changed the last category from full and partial antagonists to functional agonists/antagonists, who produce different signaling transduction than the endogenous or reference agonist, whichever that may be. The "inverse agonist" will cause the contrary of what the agonist is supposed to.
There are at least 7 (!) different intracellular signaling pathways currently known, which are (in)activated via CB1/CB2:
Now, if we take the endocannabinoids as reference ligands (because they are the natural ones), then THC is a partial agonist at CB1, causing more or less the same intracellular reaction but to a smaller degree.
The members of the AAI-family are to some extend partial agonists, others are rather full agonists (...being able to induce spectular panic attacks).
Rimonabant is what can be called a true inverse agonist, ie. it acts on the same pathways like the endocannabinoids but in the opposite direction. See eg this:
from: International Journal of Obesity (2009) 33: 947–955
DOI:10.1038/ijo.2009.132
...which is the recommended readiung on this topic!
I would still changed the last category from full and partial antagonists to functional agonists/antagonists, who produce different signaling transduction than the endogenous or reference agonist, whichever that may be. The "inverse agonist" will cause the contrary of what the agonist is supposed to.
There are at least 7 (!) different intracellular signaling pathways currently known, which are (in)activated via CB1/CB2:
* coupling to adenylate cyclase; the in vitro measured parameter to detect if this pathways is adressed is usually binding of [35S]GTPγS
* modulation of Ca2+ channels (inhibiting influx) via modulation of phospholiphase activity (= release of IP3)
* modulation of inwardly rectifying K+ channels (valif for CB1, but not CB2)
* hydrolysis of sphingomyelin (valid for CB1)
* activation of the Raf-1/MEK/ERK-cascasde
* activation of the JNK and p38 kinase pathways (mainly via CB2 IIRC)
* upregulation of certain transcription factors (Krox 24, Fos, brain-derived neurotrophic factor)
* modulation of Ca2+ channels (inhibiting influx) via modulation of phospholiphase activity (= release of IP3)
* modulation of inwardly rectifying K+ channels (valif for CB1, but not CB2)
* hydrolysis of sphingomyelin (valid for CB1)
* activation of the Raf-1/MEK/ERK-cascasde
* activation of the JNK and p38 kinase pathways (mainly via CB2 IIRC)
* upregulation of certain transcription factors (Krox 24, Fos, brain-derived neurotrophic factor)
Now, if we take the endocannabinoids as reference ligands (because they are the natural ones), then THC is a partial agonist at CB1, causing more or less the same intracellular reaction but to a smaller degree.
The members of the AAI-family are to some extend partial agonists, others are rather full agonists (...being able to induce spectular panic attacks).
Rimonabant is what can be called a true inverse agonist, ie. it acts on the same pathways like the endocannabinoids but in the opposite direction. See eg this:
from: International Journal of Obesity (2009) 33: 947–955
DOI:10.1038/ijo.2009.132
...which is the recommended readiung on this topic!
