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OD Moderators: Keif’ Richards | Tryptamino
Caffeine
- Thread starter wikings
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silverfucked
Bluelighter
Caffeine?
This was the chem that started my entire drug carreer. At age 13 I was drinking multiple large glasses of expresso and milk. I would draw and write epic novels all night.
Ten years later 800 milligrams worth of caffiene in No-Doz (and a few Red Bulls) in a day is no problem as far as side-effects, but I still love it for long drives, thinking, creativity, running, just feeling sharp, confident, witty, and interested in reality. (puffing herb should negate any nausea or jitters).
I have a feeling if I were to move on to more hardcore stimulants I would soon become a crazed meth junkie and die quickly, since I would like it too much. I'll stick to caffeine.
This was the chem that started my entire drug carreer. At age 13 I was drinking multiple large glasses of expresso and milk. I would draw and write epic novels all night.
Ten years later 800 milligrams worth of caffiene in No-Doz (and a few Red Bulls) in a day is no problem as far as side-effects, but I still love it for long drives, thinking, creativity, running, just feeling sharp, confident, witty, and interested in reality. (puffing herb should negate any nausea or jitters).
I have a feeling if I were to move on to more hardcore stimulants I would soon become a crazed meth junkie and die quickly, since I would like it too much. I'll stick to caffeine.
PhreeX
Bluelight Crew
Heroin sure as hell wakes me up more then caffeine .. of course at a large dose I will nod but at yer regular dose I can go from dead tired to wide awake...
Arghh...so much misinformed info masquerading as fact. Gasbo did a good job with most of it but I feel compelled to mention a few points he skimmed over BTW the question of whether heroin affects dopamine seemed to be largely semantical. None of the normal opiates (don't know if crazy shit like apomorphine count) directly affect dopamergenic nuerons. However, a secondary effect does increase dopamine in specific regions. So they can only be said to affect dopamine in so far as things like video games (which have been shown to increase dopamine in the same areas) can be.
I just wanted to mention that whoever was talking about the action of amphetamines was mostly right. Amphetamines have three (or four depending on how you count) significant effects on monoamines.
1) They block reuptake (most significant effect at lower doses).
2) They cause the monoamine to leak out of its vesicle inside the cell and cause the relevant reuptake transporter to reverse pumping the NT out of the cell. The mechanisms involved here don't seem to be fully understood yet.
3) And I think this is the most minor of the effects. They can function as MAOIs.
In short the action of amphetamines (and even things like ritalin which seems to mostly just block reuptake) resembles the action of caffeine in no way.
Also gasbo are you sure caffeine is a vasioconstrictor? For some reason I thought it was a dilater like nicotine.
Interestingly enough it seems that the mu opiod receptors primary effect is to inhibit cAMP formation in those cells. Just goes to show you that NT levels arent everything, alot has to do with which areas it affects. Also ritalin is nearly as effective in cocaine at blocking DA reuptake yet most people report that it is nowhere near as euphoric. The two explanations which seem credible are either the sodium channel action of cacaine is significant (some recent studies have shown that cocaine actually causes release as well...not sure what the mechanism is here..might even be indirect for all I know). Also there are some areas in the brain where dopamine release is avoided by animals (opposite of self-admin). Cocaine and ritalin do seem to have significantly differnt distributions of dopamine reuptake inhibition. Ohh shit forgot the most likely third possibility which was the result of a study correlating subjective liking to ratio of dopamine to norep released. Okay will stop blabbering now.
[ 11 August 2002: Message edited by: quale ]
I just wanted to mention that whoever was talking about the action of amphetamines was mostly right. Amphetamines have three (or four depending on how you count) significant effects on monoamines.
1) They block reuptake (most significant effect at lower doses).
2) They cause the monoamine to leak out of its vesicle inside the cell and cause the relevant reuptake transporter to reverse pumping the NT out of the cell. The mechanisms involved here don't seem to be fully understood yet.
3) And I think this is the most minor of the effects. They can function as MAOIs.
In short the action of amphetamines (and even things like ritalin which seems to mostly just block reuptake) resembles the action of caffeine in no way.
Also gasbo are you sure caffeine is a vasioconstrictor? For some reason I thought it was a dilater like nicotine.
Interestingly enough it seems that the mu opiod receptors primary effect is to inhibit cAMP formation in those cells. Just goes to show you that NT levels arent everything, alot has to do with which areas it affects. Also ritalin is nearly as effective in cocaine at blocking DA reuptake yet most people report that it is nowhere near as euphoric. The two explanations which seem credible are either the sodium channel action of cacaine is significant (some recent studies have shown that cocaine actually causes release as well...not sure what the mechanism is here..might even be indirect for all I know). Also there are some areas in the brain where dopamine release is avoided by animals (opposite of self-admin). Cocaine and ritalin do seem to have significantly differnt distributions of dopamine reuptake inhibition. Ohh shit forgot the most likely third possibility which was the result of a study correlating subjective liking to ratio of dopamine to norep released. Okay will stop blabbering now.
[ 11 August 2002: Message edited by: quale ]
Also gasbo are you sure caffeine is a vasioconstrictor? For some reason I thought it was a dilater like nicotine.
Caffeine's effects on the Cardiovascular system are largely confined to the heart, and vascular effects are only seen with high experimental in vivo concentrations of the drug. The Methyl xanthine (PDEI) effect on the heart is related to the positive inotrophy and positive chronotrophy. In high (READ: experimental doses) it is a vasoconstrictor mediated by increased levels of cAMP in the cytoplasm of the smooth muscle cells of the media.
As for being like Nictotine, 2 points:
(i) Vasoconstrictor
(ii) Mechanism of action.
Different mechanism of action entirely and again - Nictoines main action on the vascular system is secondary to its stimulation within the sympathetic ganglia (especially the biggest and best - albeit modified sympathetic ganglia: the Adrenal gland) - leading to adrenaline and noradrenaline release. It is the adrenaline and noradrenaline responsible for the vasoconstriction afforded by nicotine.
All opioid receptors are inhibitory.
By and large yes - this is true - however what is interesting about the inhibition is the mechanisms. There are many opioid receptors described as we all know. This has been further complicated in 1997 when some twits from the International Union on Pharmacology decided to reclassify opioid receptors in OP1 (formerly delta), OP2 (formerly kappa), and OP3 (formerly mu). (See BJA 7/78;81(1)1-2)
While this new classification is considered the more accurate and descriptive and even postulated an M3G receptor as well, I guess old pharmacology thought still 'dies hard' and the mu, kappa, delta etc persists in most of our minds.
The opioid receptors are G protein coupled ion channels and decrease neurotransmission (presynaptically more so than post-synaptically).
The G1i protein inhibits adenylyl cyclase leading to reduced cAMP. In mu1 and delta systems this leads to opening Potassium channels, hyperpolarising the membrane. In kappa systems, it leads to closure of calcium channels, and again hyperpolarising the membrane.
Just thought I would complicate things further and broaden the discussion
BTW - Wilson : That is a great archive of neurobiology and pharmacology ... am going to start working my way through them over the next few days - thanks ! Can never have too much information, especially when it is referenced so well and also published (ie. subject to peer review!)
[ 13 August 2002: Message edited by: gasbo ]
Hmm..what I was thinking of was some studies which showed nicotine increased blood flow to some parts of the brain. I thought there were some similar studies with caffeine.
I guess this in no way implies they are vascodialaters, probably most stimulants increase blood flow to regions of the brain b/c of their stimulator effects (i.e. blood flow increases when that part of the brain needs more oxygen).
I guess this in no way implies they are vascodialaters, probably most stimulants increase blood flow to regions of the brain b/c of their stimulator effects (i.e. blood flow increases when that part of the brain needs more oxygen).