Quote (Balla @ Oct 5 2014 10:55pm)
Yeah I don't really see a problem with it
Unfortunately I'm having a hard time predicting complete interactions.. mostly because the brain is just so much more complex than other bodily areas in terms of receptor distribution, differential effects, location on the post synaptic neuron itself, etc.
I can say, both are going to be largely inhibitory. Your antidepressant drug is melatonergic aka it activates melatonin receptors, mimicking that action. Of course cannabis is largely inhibitory. They've both, independently been found to increase neurogenesis, so that could possibly be augmented. I couldn't imagine it be negated tbh. Cannabis has anti-depressant effects on its own anyway, and I've heard MANY anecdotes of using cannabis with their SSRI or other antidepressant ameliorating symptoms to a greater degree.
Though cannabis is generally an antidepressant, euphoric, etc, in excess it can be purely negative in terms of its effect on depression. That's because one of the MAIN brain areas usually dysregulated in depressed patients is the anterior cingulate cortex.. if you were to smoke for literally years with a very heavy dose (5+ blunts a day), that area could shrink. If used intermittently and in smaller doses, it actually augments activation of that area, attributing part of its antidepressant effect, which also comes from its increase in neurogenesis.
Anotther aspect to keep in mind is the location of the receptors.. cannabinoid receptors are almost uniformly expressed on the presynaptic endings, whereas melatonin are mostly on postsynaptic neurons I believe, with some located on certain presynaptic regions. For that reason, I don't really feel too comfortable recommending something that hasn't been actually tested. You really never know until an actual study comes along with something this complex.
Sorry for disappointing this time haha. Plus I'm kind of out of it so I can't critically think right now.
Oh and btw, that bit about serotonin and depression is pretty much nonsense. Any sort of monoamine hypothesis is silly.
Really, in terms of the etiology of depression, it seems that it doesn't BEGIN out of some inbalance in neurotransmitters or some small brain region. It typically begins due to some type of low grade systemic inflammation or stress. There's just inherent genetic predispositions to how you handle the stress.. genetically predisposed to not handle stress well usually causes depression. Same for the inflammation.
It seems that AFTER the depression has begun is when the deleterious cascades occur, such as impaired neurogenesis, hippocampal atrophy, perturabations in certain brain regions, sometimes (not as often) shifts in neurotransmission, etc. That's when it becomes difficult to reverse and treat, but that takes some time.
That's where anti-depressants come in. SSRIs don't work due to increasing serotonin, they work after 3-4 weeks due to enhancing neurogenesis, synaptogensis, and overall neuronal survival and neurite outgrowth.
So if I just take an anti inflammatory, such as advil, my depression will lesson?