R3l@X
Well-Known Member
U must have the worst comedowns/hangovers
The UK Growers Thread!
- Thread starter lozac123
- Start date
tbh i aint mate, i dont really get that hungover very pissed off mind but not hungover lol thats a plus i spose....
Saerimmner
Well-Known Member
Morning all, another year older.......bollocks
happy fathers day to all my fellow child sufferers lol
happy fathers day to all my fellow child sufferers lol
laptop is working thank fuck, no more lines mate no more booze, i had a liver n kidney function test a few wks ago results for the liver function werent great as to be expected i spose lol
of course i rang em last night, but carnt imagine i sounded like the most sane of people n was just longed off.......
Saerimmner
Well-Known Member
Found this, might be a decent read for someone lol
Everything you wanted to know about cannabinoids: Pharmacology of THC
By Matthew Lazenka | June 13th 2014 02:01 PM | Print | E-mail | Track Comments
Internal struggle of the mind
More Articles
About Matthew
I am a postdoctoral fellow who received a PhD in neuroscience in 2013. My PhD research focused on the long-term effects of THC....
View Matthew's Profile
Matthew Lazenka Most of you are likely aware that THC is the chemical in marijuana that gets you “high,” thus it is considered the main “psychoactive” constituent of marijuana. Roger Adams first isolated the constituents of marijuana in the 1940s, but it was not until the 1960s that Mechoulam and Gaoni determined the structure for THC.
This article’s focus is on the pharmacology of THC and its effects on one aspect of the endogenous cannabinoid system. The primary mechanism of action by which THC produces its psychoactive effects is the cannabinoid type 1 (CB1) receptor, whereas the CB2 receptor is mostly involved in immune function and deserves its own discussion.
The evidence for the action of THC at CB1 receptors has been demonstrated by using antagonists against the CB1 receptor (molecules that bind to the receptor, but don’t increase signaling). These studies primarily use Rimonabant (SR141716A), which was pulled from shelves in Europe because it caused suicidal ideations (among other things), or through genetic removal of CB1 receptors in mice, i.e. CB1 receptor knockout mice.
I just want to note that Rimonabant is technically an inverse agonist, which means it reduces constitutive activity at the CB1 receptor. A rather surprising fact about THC is that it is a partial agonist, meaning, it does not produce much signaling at the CB1 receptor when compared to both endogenous ligands such as 2-AG and anadamide nor the synthetic ligands such as WIN55,212-2 or CP55,940.
The spice compounds, which are more available now, such as CP 47,497-C8, also have higher efficacy and potency compared to THC. The figure below (PMID: 8987831) demonstrates this point regarding both the efficacy and potency of THC.
Figure 1. THC is a partial agonist as it produces much less G-protein signaling in the rat brain compared to the full agonist WIN55,212-2. Another hallmark of partial agonists is that they reduce the signaling of full agonists when added in combination with full agonists (the open symbols in the graph).
This is why low efficacy, partial agonists, for which THC is defined as, act as antagonists in some assays. In fact, it would be expected that THC would reduce endogenous cannabinoid signaling. Also notice that THC is less potent than WIN55,212-2 as more THC is necessary to produce a maximum effect. Remember, potency has nothing to do with the effect of a drug, unless, of course, you read any media discussions of potency.
This leads me to introduce the different classes of cannabinoids, as presented in the figure below.
Figure 2. A) the phytocannabinoids that are derived from marijuana, B) some synthetic cannabinoids, C) the endogenous cannabinoids, D) the antagonist Rimonabant and E) the spice compounds.As you can gather, cannabinoids are mostly lipid in nature, which means they cross the blood/brain barrier easily and are stored in fat. This aspect of cannabinoids caused early researchers to suggest initially that cannabinoids disrupted cell membranes instead of acting at receptors. However, in the 1980s, Howlett discovered that cannabinoids acted at G-protein receptors through a pertussis toxin sensitive mechanism. These receptors, namely CB1 and CB2, were discovered by Matsuda and Munro in the early 1990s. This discovery led to the creation of CB1 knockout mice (PMID 10318961), which helped to further strengthen the role of CB1 receptors as the major contributors to the behavioral effects produced by cannabinoids.
More recent studies from Dr. Nora Volkow, the head of the National Institute on Drug Abuse (NIDA), have used positron emission topography (PET) imaging and an antagonist FMPEP-d2 with a radioactive fluorine [18F] to measure cannabinoid receptors in human marijuana users and non-users (PMID:2174739
.
This study demonstrated that human marijuana users demonstrate a decrease in CB1 receptors, suggesting that repeated THC exposure decreases CB1 receptor protein levels in various brain regions.
Although this phenomenon is well known to occur in various animals, with most studies focusing on rodents, this study was the first real-time visualization in living subjects. A figure from the paper is depicted below.
Figure 3. Relative decrease in CB1 receptors in marijuana users in cortical regions compared to non-users.In conclusion, THC is a low efficacy, partial agonist which is the main psychoactive constituent of marijuana. Its effects are mediated primarily through CB1 receptors. Repeated marijuana use can decrease the expression of CB1 receptors, but the consequences of this are not fully understood. Spice compounds, unlike THC, have much higher efficacy and potency, which explains why these compounds produce stronger “highs” than THC, as per Erowid discussions.
In conclusion, THC is a low efficacy, partial agonist which is the main psychoactive constituent of marijuana. Its effects are mediated primarily through CB1 receptors. Repeated marijuana use can decrease the expression of CB1 receptors, but the consequences of this are not fully understood.
Spice compounds, unlike THC, have much higher efficacy and potency, which explains why these compounds produce stronger “highs” than THC, as per Erowid discussions.
http://www.science20.com/internal_struggle_of_the_mind/blog/everything_you_wanted_to_know_about_cannabinoids_pharmacology_of_thc-138539
Everything you wanted to know about cannabinoids: Pharmacology of THC
By Matthew Lazenka | June 13th 2014 02:01 PM | Print | E-mail | Track Comments
Internal struggle of the mind
More Articles
- Everything you wanted to know about cannabinoids: Pharmacology of THC
- The Healthcare Law Is Definitely Not Working As Proposed
- Everything you wanted to know about cannabinoids: What are cannabinoids?
About Matthew
I am a postdoctoral fellow who received a PhD in neuroscience in 2013. My PhD research focused on the long-term effects of THC....
View Matthew's Profile
This article’s focus is on the pharmacology of THC and its effects on one aspect of the endogenous cannabinoid system. The primary mechanism of action by which THC produces its psychoactive effects is the cannabinoid type 1 (CB1) receptor, whereas the CB2 receptor is mostly involved in immune function and deserves its own discussion.
The evidence for the action of THC at CB1 receptors has been demonstrated by using antagonists against the CB1 receptor (molecules that bind to the receptor, but don’t increase signaling). These studies primarily use Rimonabant (SR141716A), which was pulled from shelves in Europe because it caused suicidal ideations (among other things), or through genetic removal of CB1 receptors in mice, i.e. CB1 receptor knockout mice.
I just want to note that Rimonabant is technically an inverse agonist, which means it reduces constitutive activity at the CB1 receptor. A rather surprising fact about THC is that it is a partial agonist, meaning, it does not produce much signaling at the CB1 receptor when compared to both endogenous ligands such as 2-AG and anadamide nor the synthetic ligands such as WIN55,212-2 or CP55,940.
The spice compounds, which are more available now, such as CP 47,497-C8, also have higher efficacy and potency compared to THC. The figure below (PMID: 8987831) demonstrates this point regarding both the efficacy and potency of THC.
Figure 1. THC is a partial agonist as it produces much less G-protein signaling in the rat brain compared to the full agonist WIN55,212-2. Another hallmark of partial agonists is that they reduce the signaling of full agonists when added in combination with full agonists (the open symbols in the graph).
This is why low efficacy, partial agonists, for which THC is defined as, act as antagonists in some assays. In fact, it would be expected that THC would reduce endogenous cannabinoid signaling. Also notice that THC is less potent than WIN55,212-2 as more THC is necessary to produce a maximum effect. Remember, potency has nothing to do with the effect of a drug, unless, of course, you read any media discussions of potency.
This leads me to introduce the different classes of cannabinoids, as presented in the figure below.
Figure 2. A) the phytocannabinoids that are derived from marijuana, B) some synthetic cannabinoids, C) the endogenous cannabinoids, D) the antagonist Rimonabant and E) the spice compounds.As you can gather, cannabinoids are mostly lipid in nature, which means they cross the blood/brain barrier easily and are stored in fat. This aspect of cannabinoids caused early researchers to suggest initially that cannabinoids disrupted cell membranes instead of acting at receptors. However, in the 1980s, Howlett discovered that cannabinoids acted at G-protein receptors through a pertussis toxin sensitive mechanism. These receptors, namely CB1 and CB2, were discovered by Matsuda and Munro in the early 1990s. This discovery led to the creation of CB1 knockout mice (PMID 10318961), which helped to further strengthen the role of CB1 receptors as the major contributors to the behavioral effects produced by cannabinoids.
More recent studies from Dr. Nora Volkow, the head of the National Institute on Drug Abuse (NIDA), have used positron emission topography (PET) imaging and an antagonist FMPEP-d2 with a radioactive fluorine [18F] to measure cannabinoid receptors in human marijuana users and non-users (PMID:2174739
. This study demonstrated that human marijuana users demonstrate a decrease in CB1 receptors, suggesting that repeated THC exposure decreases CB1 receptor protein levels in various brain regions.
Although this phenomenon is well known to occur in various animals, with most studies focusing on rodents, this study was the first real-time visualization in living subjects. A figure from the paper is depicted below.
Figure 3. Relative decrease in CB1 receptors in marijuana users in cortical regions compared to non-users.In conclusion, THC is a low efficacy, partial agonist which is the main psychoactive constituent of marijuana. Its effects are mediated primarily through CB1 receptors. Repeated marijuana use can decrease the expression of CB1 receptors, but the consequences of this are not fully understood. Spice compounds, unlike THC, have much higher efficacy and potency, which explains why these compounds produce stronger “highs” than THC, as per Erowid discussions.
In conclusion, THC is a low efficacy, partial agonist which is the main psychoactive constituent of marijuana. Its effects are mediated primarily through CB1 receptors. Repeated marijuana use can decrease the expression of CB1 receptors, but the consequences of this are not fully understood.
Spice compounds, unlike THC, have much higher efficacy and potency, which explains why these compounds produce stronger “highs” than THC, as per Erowid discussions.
http://www.science20.com/internal_struggle_of_the_mind/blog/everything_you_wanted_to_know_about_cannabinoids_pharmacology_of_thc-138539
i have issues mate that no amount of tissues are gonna solve lol
im a addict n my names sam lmfao better to laugh than cry i spose....
Hydrogrow123
Well-Known Member
Vodkas probly one of the worser things u could drink too. I left an iphone In a taxi once, when I rang them the guys says next run he's doin near mine he'd drop it in and he did. Can't see much luck with a half of weed tho
R3l@X
Well-Known Member
Ah man ur making me regret ordering that coke now lol
Hydrogrow123
Well-Known Member
U only ordered it for research did u not? Well send it up here then and I'll tell u what it's like....research done
R3l@X
Well-Known Member
You're right bud, since I'm taking.it for science it should be fine...FOR SCIENCE
R3l@X
Well-Known Member
Nah mate n ur bang on lol looking forward to the difference between the fishy cola n the pharma...following vice on Facebook...had no idea how much shot they've done but the lad on acid at the dog show has to be in my top5. Tech hippy pricy but imma be getting few g's of each his stuff after I'm done trying the coke...wanna get some edibles 2
zeddd
Well-Known Member
good morning, Rambo mate whatcha doin....2 bottlesffffs... any mate of yours should tell you....tooooo fukin much mate even your body cant take that, theres a lotta love for you man don't go jillin yaself cos whose gonna be bringing up your kids and getting called dad, not you if u in a box in the synagogue
zeddd
Well-Known Member
Found this, might be a decent read for someone lol
Everything you wanted to know about cannabinoids: Pharmacology of THC
By Matthew Lazenka | June 13th 2014 02:01 PM | Print | E-mail | Track Comments
Internal struggle of the mind
More Articles
All Articles
- Everything you wanted to know about cannabinoids: Pharmacology of THC
- The Healthcare Law Is Definitely Not Working As Proposed
- Everything you wanted to know about cannabinoids: What are cannabinoids?
About Matthew
I am a postdoctoral fellow who received a PhD in neuroscience in 2013. My PhD research focused on the long-term effects of THC....
View Matthew's Profile
Matthew Lazenka Most of you are likely aware that THC is the chemical in marijuana that gets you “high,” thus it is considered the main “psychoactive” constituent of marijuana. Roger Adams first isolated the constituents of marijuana in the 1940s, but it was not until the 1960s that Mechoulam and Gaoni determined the structure for THC.
This article’s focus is on the pharmacology of THC and its effects on one aspect of the endogenous cannabinoid system. The primary mechanism of action by which THC produces its psychoactive effects is the cannabinoid type 1 (CB1) receptor, whereas the CB2 receptor is mostly involved in immune function and deserves its own discussion.
The evidence for the action of THC at CB1 receptors has been demonstrated by using antagonists against the CB1 receptor (molecules that bind to the receptor, but don’t increase signaling). These studies primarily use Rimonabant (SR141716A), which was pulled from shelves in Europe because it caused suicidal ideations (among other things), or through genetic removal of CB1 receptors in mice, i.e. CB1 receptor knockout mice.
I just want to note that Rimonabant is technically an inverse agonist, which means it reduces constitutive activity at the CB1 receptor. A rather surprising fact about THC is that it is a partial agonist, meaning, it does not produce much signaling at the CB1 receptor when compared to both endogenous ligands such as 2-AG and anadamide nor the synthetic ligands such as WIN55,212-2 or CP55,940.
The spice compounds, which are more available now, such as CP 47,497-C8, also have higher efficacy and potency compared to THC. The figure below (PMID: 8987831) demonstrates this point regarding both the efficacy and potency of THC.
Figure 1. THC is a partial agonist as it produces much less G-protein signaling in the rat brain compared to the full agonist WIN55,212-2. Another hallmark of partial agonists is that they reduce the signaling of full agonists when added in combination with full agonists (the open symbols in the graph).
This is why low efficacy, partial agonists, for which THC is defined as, act as antagonists in some assays. In fact, it would be expected that THC would reduce endogenous cannabinoid signaling. Also notice that THC is less potent than WIN55,212-2 as more THC is necessary to produce a maximum effect. Remember, potency has nothing to do with the effect of a drug, unless, of course, you read any media discussions of potency.
This leads me to introduce the different classes of cannabinoids, as presented in the figure below.
Figure 2. A) the phytocannabinoids that are derived from marijuana, B) some synthetic cannabinoids, C) the endogenous cannabinoids, D) the antagonist Rimonabant and E) the spice compounds.As you can gather, cannabinoids are mostly lipid in nature, which means they cross the blood/brain barrier easily and are stored in fat. This aspect of cannabinoids caused early researchers to suggest initially that cannabinoids disrupted cell membranes instead of acting at receptors. However, in the 1980s, Howlett discovered that cannabinoids acted at G-protein receptors through a pertussis toxin sensitive mechanism. These receptors, namely CB1 and CB2, were discovered by Matsuda and Munro in the early 1990s. This discovery led to the creation of CB1 knockout mice (PMID 10318961), which helped to further strengthen the role of CB1 receptors as the major contributors to the behavioral effects produced by cannabinoids.
More recent studies from Dr. Nora Volkow, the head of the National Institute on Drug Abuse (NIDA), have used positron emission topography (PET) imaging and an antagonist FMPEP-d2 with a radioactive fluorine [18F] to measure cannabinoid receptors in human marijuana users and non-users (PMID:2174739
This study demonstrated that human marijuana users demonstrate a decrease in CB1 receptors, suggesting that repeated THC exposure decreases CB1 receptor protein levels in various brain regions.
Although this phenomenon is well known to occur in various animals, with most studies focusing on rodents, this study was the first real-time visualization in living subjects. A figure from the paper is depicted below.
Figure 3. Relative decrease in CB1 receptors in marijuana users in cortical regions compared to non-users.In conclusion, THC is a low efficacy, partial agonist which is the main psychoactive constituent of marijuana. Its effects are mediated primarily through CB1 receptors. Repeated marijuana use can decrease the expression of CB1 receptors, but the consequences of this are not fully understood. Spice compounds, unlike THC, have much higher efficacy and potency, which explains why these compounds produce stronger “highs” than THC, as per Erowid discussions.
In conclusion, THC is a low efficacy, partial agonist which is the main psychoactive constituent of marijuana. Its effects are mediated primarily through CB1 receptors. Repeated marijuana use can decrease the expression of CB1 receptors, but the consequences of this are not fully understood.
Spice compounds, unlike THC, have much higher efficacy and potency, which explains why these compounds produce stronger “highs” than THC, as per Erowid discussions.
http://www.science20.com/internal_struggle_of_the_mind/blog/everything_you_wanted_to_know_about_cannabinoids_pharmacology_of_thc-138539[/QUOTE]ta sae he wasted his time with this dyk?