Yeah the chart might seem a bit overwhelming at the first glance, but its not that difficult to comprehend once you realize the roles of the receptors and ions involved in the activity of various receptor ligands. So let me break it down for you to as how I see and understand it:
Ca2+ ions are initiators of neural transmissions, Calcium ion influx is generally the first step behind the liberation of neurotransmitters (such as Serotonin, Nor-Adrenaline, Glutamate and many more) from their center of residence (synaptic vesicle in the presynaptic neurone) into the synaptic cleft where they bind to the receptor sites of the post-synaptic neuron which then elicits a corresponding physiological response. Therefore the decrease in Ca2+ (as CBD does according to the chart) will result in less transmission, which can alleviate possible excitotoxicity (too much transmission at excitatory synapses can have neurotoxic effects: e.g excess release of glutamate in depressed patients) thus will serve a neuro-protective role in this case.
5HT1A (+) indicates that CBD is an agonist at the serotonin receptor labeled as 5HT1A. The same action exhibits buspirone, which is an anxiolytic and anti-depressant. (-) Would indicate an antagonist.
FAAH (arrow down) indicates that CBD has suppressing effects on the Fatty Acid Amide Hydrolase, which breaks down endogenous (naturally occurring in our bodies) anandamide, a compound having affinity for the cannabinoid receptors. Therefore CBD allows for less anandamide to be broken down thus more is available for binding to the corresponding receptors (CB1). From this we can see that CBD does indeed activate the CB receptors, but not by directly binding to them as it has no affinity for these receptor sites.
TRPV1 (+) means that CBD acts as an agonist on that receptor. This particular receptor is involved in pain perception, body temperature and inflammation (agonists affect these aspects positively meaning that pain threshold rises, temperature drops and inflammation is attenuated). Hot foods comprised of chilli (contains capsaicin) also elicit activation of this receptor, that is why spicy foods may have pain-relieving properties.
Adenosine Uptake (arrow down) means that that the uptake of the adenosine receptor ligand into the post-synaptic neuron is inhibited allowing the transmitter to remain in the synaptic cleft for a longer time (where it gets to activate the adenosine receptors). Adenosine receptor is thought to be implicated in anxiety, agonists having an anxiolytic effect. It is also involved in inflammation as the chart indicates.
T-cells (arrow down) indicates the decrease in the activity of this particular type of lymphocytes resulting in immuno-suppressive effects which may be beneficial to people suffering from auto-immune diseases such as cancer.
GABA (arrow down) next to THCV indicates the down-regulating effect on GABA transmitter (main inhibitory neurotransmitter). I am still working on making sense out of this particular example because logically I would expect increase in GABA transmission to induce anti-epileptic effects (as benzodiazepines do). However receptors work in a much more intricate way than is commonly thought so I would guess the proposed mechanism involves decreased binding at the GABA autoreceptors which would increase the release of GABA into the synaptic cleft thus facilitating anti-epileptic properties.
The CB1 (-): antagonistic effect of THCV on this cannabinoid receptor has anorectic properties. I would say this is simply because agonists induce hunger so antagonists will eliminate this response.
If you see any mistakes please correct me and feel free to make any additions as I would like to avoid making erroneous assumptions and generally am interested in the exact mechanisms of action behind the various cannabinoids. I will look deeper into the concepts of which I am not so sure about and edit/update this post accordingly.
