...no, they act on different receptors to the best of my knowledge.
I've quoted some research in this thread and the other one.
"But how is marijuana addictive? What’s the link to heroin?
What most people don’t know is that there is quite a bit of interaction between the cannabinoid receptor system (especially CB1 receptors) and the opioid receptor system in the brain. In fact, research has shown that without the activation of the µ opioid receptor, THC is no longer rewarding.
If the fact that marijuana activates the same receptor system as opiates (like heroin, morphine, oxycontin, etc.) ....
etc etc etc...
Funken, funken, funken.... WTF?
I was addressing this statement here.
funken wrote:They all act on the same brain receptors and reward pathways in fact.
Yes, they do
influence the reward pathways, but (now please, pay attention to this simple thing I am saying here) they act on different receptors
. Not only that but they also affect the reward pathways in different complex ways - I know it is being pedantic, but surely there is nothing wrong with clarifying so-called 'facts'. You can refer to other documents, 'research' and what have you stating 'same receptors' all you like, but it will not change simple established knowledge of neurophysiology, neurotransmitters and the physiology of cell membranes, transport mechanisms, receptors, agonists and antagonists. I just don't like 'fuzzy' science.
I stand by my other statements regarding addictions as well. These issues are often far too complex to solve every individuals addiction problems through answers provided in any one book or approach...
Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors.
Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.
The reason that opiates such as heroin and morphine affect us so powerfully is that these exogenous substances bind to the same receptors as our endogenous opioids. There are three kinds of receptors widely distributed throughout the brain: mu, delta, and kappa receptors.
These receptors, through second messengers, influence the likelihood that ion channels will open, which in certain cases reduces the excitability of neurons. This reduced excitability is the likely source of the euphoric effect of opiates and appears to be mediated by the mu and delta receptors.
This euphoric effect also appears to involve another mechanism in which the GABA-inhibitory interneurons of the ventral tegmental area come into play. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released. Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt.
Cocaine acts by blocking the re-uptake of certain neurotransmitters such as dopamine, norepinephrine, and serotonin.
By binding to the transporters that normally remove the excess of these neurotransmitters from the synaptic gap, cocaine prevents them from being reabsorbed by the neurons that released them and thus increases their concentration in the synapses. As a result, the natural effect of dopamine on the post-synaptic neurons is amplified. The group of neurons thus modified produces much more dependency (from dopamine), feelings of confidence (from serotonin), and energy (from norepinephrine) typically experienced by people who take cocaine.
Nicotine imitates the action of a natural neurotransmitter called acetylcholine and binds to a particular type of acetylcholine receptor, known as the nicotinic receptor.
Whether it is acetylcholine or nicotine that binds to this receptor, it responds in the same way: it changes its conformation, which causes its associated ion channel to open for a few milliseconds. This channel then allows sodium ions to enter the neuron, depolarizing the membrane and exciting the cell. Then the channel closes again, and the nicotinic receptor becomes temporarily unresponsive to any neurotransmitters. It is this state of desensitization that is artificially prolonged by continual exposure to nicotine.
Tobacco dependency, which then develops very quickly, arises because nicotinic receptors are present on the neurons of the ventral tegmental area which project their terminations into the nucleus accumbens. In smokers, repeated nicotine stimulation thus increases the amount of dopamine released in the nucleus accumbens. Between cigarettes, however, chronic smokers maintain a high enough concentration of nicotine to deactivate the receptors and slow down their recovery. This is why smokers develop a tolerance to nicotine and experience reduced pleasure from it.
The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain
. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body’s natural morphines.
Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.
THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain’s neural networks is thus reduced as well.
However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.