to be clear, any intelligent discussion of activating receptors and NEGATIVE side effect are largely discounted by people who romanticize the plant..ie people on a weed site... however we love to talk about POSITIVE side effects from hitting the same receptors lol funny how we think yiu can have one but not the other
thc used to be widely known as hallucinogen, depressant AND stimulant.
this only occurs in new users. once you gain a tolerance, pop site density lowers to a level where thc- a partial agonist and can take up more space than it activates causing antagonism instead of agonism...essentially . in new users it can act like the much more potent full agonist jwh018 we are familiar with. but even after prolonged tolerance break, this sits density does not return to complete baseline.
funny how many people will tell you they had mild auditory or closed eye visuals on cannabis when they first started but attribute it to tainted weed haha... yea i hallucinated, my friends did, my pops did, my patients and study groups do as well when new
so threads like this inevitably end in a poo tornado...no shit this wont happen to someone whos been smoking for 30 years and feels they understand the affect.
i however work with new patients all the time... edibles can also do this with intensity
if your actually looking for info id be glad to provide it in detail..
i didnt post as i assumed, if your english is terrible you most likely wouldnt comprehend what im saying
because most people dont understand the pharmacology this discussion will go no where
cannabis- thc hits the sites i mentioned, which are responsible for the affects of dissociatives and hallucinogens.
if your personal site density is altered, say your sick or depressed which can change 5ht (serotonin) this makes a difference
looking at the structure of thc we can estimate(with accuracy) and through testing know what sites it will hit and how effectively. roughly 20 are being hit when smoking cannabis.
look into the mentioned sites with specific attention to 5ht2a and sigma 1
for example. (published in 2014)
Studies in humans have indicated that abuse of smoked cannabis can promote psychosis and even circumstantially precipitate symptoms of schizophrenia, although the latter appears to require a prior vulnerability in the individual. It is possible that cannabinoids provoke psychosis/schizophrenia reflecting a mechanism common to neuroprotection: the reduction of NMDAR activity. Cannabinoids are proposed to produce such effect by reducing the pre-synaptic release of glutamate or interfering with post-synaptic NMDAR-regulated signaling pathways. The efficacy of such control requires the endocannabinoid system to apply its negative influence in a manner that is proportional to the strength of NMDAR signaling. Thus, cannabinoids acting at the wrong time or exerting an inappropriate influence on their receptors may cause NMDAR hypofunction. The purpose of the present review is to draw the attention of the reader to the newly described functional and physical CB1-NMDAR association