Total mind blower. After thinking about it, im too lit to type lmao

Any more ideas folks?

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It's Medicine Jim

I was just thinking of something like this. If you get high and smoke again after 2 - 3 hours then you will get high again but for me at least it seems like I do not feel like I am getting high. I have come to the conclusion that it must be because there is no large difference. i.e when you smoke sober there is a large difference between your sober self and high self therefore you tell that you are high.

This leads me to your question. After a while you start to understand that when you are high you do act/think differently. Once you begin to understand what will change you can have a better grip on what you can and cannot do, like what that previous post said about going to the supermarket and interacting, but you also know that you cannot say write a final as easily.

So to answer more succinctly I don't believe you grow a tolerance that it doesn't affect you anymore but the first time the difference from sober to high was new, exciting and unknown. After smoking for a long while you being to understand what is going on.

P.S THC is shaped like dopamine, the chemical, or cell... that transports messages, and THC simply fits into the receptor sites preventing dopamine. If I mixed up something feel free to correct me.

Happy Toking

when and if i ever build up a tolerance ill answer that but i've been smoking off and on since the 70's so it not likely i'lll ever build a tolerance up after all this time. 3 hits and i have my high just where i want it

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A friend with weed is a friend Indeed

good question, but im not sure how to answer that one......

Heres my take...it's all mental, if you know you got "good" shit your going to think your going to get uber high and you will....

BUT

If you got some bunk bud from Johhny appleseed you will think that you wont get as high unless you smoke an 1/8 to your dome.... in all scence prolly after the first 10 hits you can't get any higher from each bud.

I agree 100% with the poster that said you need to relax and let the buzz take over.

somewhat agree with you, the first weed I got I had no clue what it was and I got fucked up! Then I discovered RIU a few years later and it turns out I was getting mids for the price of dirt(lucky me) but I thought it was dirt. It still got me hella high even though I thought it was "shitty". Now I find out its mids...

take it for what you will

The locations of the cannabinoid receptors are most revealing of the way THC acts on the brain, but the importance of this determination is best understood in comparison with the effects of other drugs on the brain. Neurons are brain cells which process information. Neurotransmitter chemicals enable them to communicate with each other by their release into the gap between the neurons. This gap is called the synapse. Receptors are actually proteins in neurons which are specific to neurotransmitters, and which turn various cellular mechanisms on or off. Neurons can have thousands of receptors for different neurotransmitters, causing any neurotransmitter to have diverse effects in the brain. Drugs affect the production, release or re-uptake (a regulating mechanism) of various neurotransmitters. They also mimic or block actions of neurotransmitters, and can interfere with or enhance the mechanisms associated with the receptor. Dopamine is a neurotransmitter which is associated with extremely pleasurable sensations, so that the neural systems which trigger dopamine release are known as the "brain reward system." The key part of this system is identified as the mesocorticolimbic pathway, which links the dopamine-production area with the nucleus of accumbens in the limbic system, an area of the brain which is associated with the control of emotion and behavior. Cocaine, for example, blocks the re-uptake of dopamine so that the brain, lacking biofeedback, keeps on producing it. Amphetamines also block the re-uptake of dopamine, and stimulate additional production and release of it. Opiates activate neural pathways that increase dopamine production by mimicking opioid-peptide neurotransmitters which increase dopamine activity in the ventral tegmental area of the brain where the neurotransmitter originates. Opiates work on three receptor sites, and in effect restrain an inhibitory amino acid, gamma-aminobutyric acid, that otherwise would slow down or halt dopamine production. All of these substances can produce strong reinforcing properties that can seriously influence behavior. The rewarding properties of dopamine are what accounts for animal studies in which animals will forgo food and drink or willingly experience electric shocks in order to stimulate the brain reward system. It is now widely held that drugs of abuse directly or indirectly affect the brain reward system. The key clinical test of whether a substance is a drug of abuse potential or not is whether administration of the drug reduces the amount of electrical stimulation needed to produce self-stimulation response, or dopamine production. This is an indication that a drug has reinforcing properties, and that an individual's use of the drug can lead to addictive and other harmful behavior. To be precise, according to the Office of Technological Assessment (OTA): "The capacity to produce reinforcing effects is essential to any drug with significant abuse potential." marijuana should no longer be considered a serious drug abuse because, as summarized by the OTA: "Animals will not self-administer THC in controlled studies . . . . Cannabinoids generally do not lower the threshold needed to get animals to self-stimulate the brain regard system, as do other drugs of abuse." marijuana does not produce reinforcing effects. The definitive experiment which measures drug-induced dopamine production utilizes microdialysis is live, freely-moving rats. Brain microdialysis has proven that opiates, cocaine, amphetamines, nicotine and alcohol all affect dopamine production, whereas marijuana does not. This latest research confirms and explains Hollister's 1986 conclusion about cannabis and addiction: "Physical dependence is rarely encountered in the usual patterns, despite some degree of tolerance that may develop." Most important, the discoveries of Howlett and Devane, Herkenham and their associates demonstrate that the cannabinoid receptors do not influence the dopamine reward system.
CANNABINOID RECEPTORS Research has enabled scientists to know which portions of the brain control various body functions, and this knowledge has been used to explain the pharmacological properties of drugs that activate receptor sites in the brain. There is a dense concentration of cannabinoid binding sites in the basal ganglia and the cerebellum of the base-brain, both of which affect movement and coordination. This discovery will aid in determining the actual physical mechanism by which THC affects spasticity and provides therapeutic benefits to patients with multiple sclerosis and other spastic disorders. While there are cannabinoid receptors in the ventromedial striatum and basal ganglia which are areas associated with dopamine production, no cannabinoid receptors have been found in dopamine-producing neurons, and as mentioned above, no reinforcing properties have been demonstrated in animal studies. There is one study by Gardner and Lowinson, involving inbred Lewis rats, in which doses of THC lowered the amount of electrical stimulation required to trigger the brain reward system. However, no one has been able to replicate the results with any other species of rat, or any other animal. The finding is believed to be the result of some inbred genetic variation in the inbred species, and is both widely mentioned in the literature and disregarded. According to Herkenham and his associates, "There are virtually no reports of fatal cannabis overdose in humans. The safety reflects the paucity of receptors in medullary nuclei that mediate respiratory and cardiovascular functions." This is also why cannabinoids have great promise as analgesics or painkillers, in that they do not depress the function of the heart or the lungs. In this respect, they are far superior to opiates, which decrease the entire physiological system because the receptors are all over the medulla as well as the brain. marijuana is distinguished from most other illicit drugs by the locations of its brain-receptor sites for two predominant reasons: (1) The lack of receptors in the medulla significantly reduces the possibility of accidental, or even deliberate, death from THC, and (2) the lack of receptors in the mesocorticolimbic pathway significantly reduces the risks of addiction and serious physical dependence. As a therapeutic drug, these features are God's greatest gifts.

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I don't grow..I just lieCheck my journal
http://www.rollitup.org/grow-journal...l-journal.html

I think I just get used to the effect of being stoned rather than building a tolerance to THC.

Maybe you can build some sort of tolerance to a particular strain, but does anyone else find that if you smoke (A) strain for say a year, it doesn't get you that high at the end of the year (or you're just more used to it) ... Then if you switch to (B) strain, you get fucked up ... Anyone else find this? ... Makes me think maybe you (or at least for me) that you don't become tolerant to the THC itself, but more used to the effect of the combination of different cannabinoids in the particular ratios in the strain you're smoking...? Maybe? Does that make sense hahaha.

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GreenX ~ Glossary of Terms:
http://www.rollitup.org/general-mari...ary-terms.html

I'm pretty sure thats already confirmed that you do build up a tolerance to a specific strain if you smoke back to back for over a couple ounces. But the tolerance goes away once you switch up strains.