Klint Finley
There is now growing evidence that cannabis use causes a small but reliable increase in the chance of developing psychosis. Traditionally, this was explained by the drug increasing dopamine levels in the brain but a new study shortly to be published in NeuroImage suggests that the active ingredient in cannabis doesn’t effect this important neurotransmitter.
Despite some dissenting voices, disruption to the mesolimbic dopamine pathway is widely thought to be the key problem in the development of delusions, hallucinations and the other psychotic symptoms commonly diagnosed as schizophrenia.
This has led to the assumption that the small increased risk of psychosis reliably associated with cannabis use is due to the drug increasing dopamine levels in a deep brain structure called the striatum.
In itself, this is partly based on another assumption - the virtual mantra of recreational drug research that ‘all drugs of abuse increase dopamine levels in the reward system’ of which the striatum is a part.
This new study, led by neuroscientist Paul Stokes, tested dopamine levels by using a type of PET brain scan where participants are injected with a radioactive tracer that binds to free dopamine receptors. Higher dopamine levels will mean that there are less free dopamine receptors and, therefore, lower tracer levels.
Mind Hacks: The straight dopamine theory could be up in smoke
Sunday, November 29, 2009
Cognitive Training Can Alter Biochemistry Of The Brain
Klint Finley
Follow-up related to the dual n-back test and its use in intelligence amplification:
Researchers at the Swedish medical university Karolinska Institutet have shown for the first time that the active training of the working memory brings about visible changes in the number of dopamine receptors in the human brain. The study, which is published in the journal Science, was conducted with the help of PET scanning and provides deeper insight into the complex interplay between cognition and the brain’s biological structure. [...]
Professor Klingberg and his colleagues have previously shown that the working memory can be improved with a few weeks’ intensive training. Through a collaborative project conducted under the Stockholm Brain Institute, the researchers have now taken a step further and monitored the brain using Positron Emission Tomography (PET scans), and have confirmed that intensive brain training leads to a change in the number of dopamine D1 receptors in the cortex.
Science Daily: Cognitive Training Can Alter Biochemistry Of The Brain
Previously: Increase your intelligence with 20mins a day brain excerise
Follow-up related to the dual n-back test and its use in intelligence amplification:
Researchers at the Swedish medical university Karolinska Institutet have shown for the first time that the active training of the working memory brings about visible changes in the number of dopamine receptors in the human brain. The study, which is published in the journal Science, was conducted with the help of PET scanning and provides deeper insight into the complex interplay between cognition and the brain’s biological structure. [...]
Professor Klingberg and his colleagues have previously shown that the working memory can be improved with a few weeks’ intensive training. Through a collaborative project conducted under the Stockholm Brain Institute, the researchers have now taken a step further and monitored the brain using Positron Emission Tomography (PET scans), and have confirmed that intensive brain training leads to a change in the number of dopamine D1 receptors in the cortex.
Science Daily: Cognitive Training Can Alter Biochemistry Of The Brain
Previously: Increase your intelligence with 20mins a day brain excerise
HOW DRUGS AFFECT NEUROTRANSMITTERS
Dopamine appeared very early in the course of evolution and is involved in many functions that are essential for survival of the organism, such as motricity, attentiveness, motivation, learning, and memorization. But most of all, dopamine is a key element in identifying natural rewards for the organism. These natural stimuli such as food and water cause individuals to engage in approach behaviours. Dopamine is also involved in unconscious memorization of signs associated with these rewards.
It has now been established that all substances that trigger dependencies in human beings increase the release of a neuromediator, dopamine, in a specific area of the brain: the nucleus accumbens. Lien: Neurobiology of addiction and implications for treatment
But not all drugs increase dopamine levels in the brain in the same way.
* Some substances imitate natural neuromediators and take their place on their receptors. Morphine, for example, binds to the receptors for endorphin (a natural "morphine" produced by the brain), while nicotine binds to the receptors for acetylcholine.
* Other substances increase the secretion of natural neuromediators. Cocaine, for example, mainly increases the amount of dopamine in the synapses, while ecstasy mainly increases the amount of serotonin.
* Still other substances block a natural neuromediator. Alcohol, for example, blocks the NMDA receptors.
Click on the names of each of the following drugs to read about how they work and what effects they have.
Alcohol ----- Opiates (heroin, morphine, etc.) ----- Cocaine ----- Nicotine
Caffeine ----- Amphetamines ----- Cannabis ----- Ecstasy ----- Benzodiazepines
Alcohol
Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.
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.
Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.
The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.
However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.
Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down.
Cannabis
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.
In chronic consumers of cannabis, the loss of CB1 receptors in the brain’s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.
It has now been established that all substances that trigger dependencies in human beings increase the release of a neuromediator, dopamine, in a specific area of the brain: the nucleus accumbens. Lien: Neurobiology of addiction and implications for treatment
But not all drugs increase dopamine levels in the brain in the same way.
* Some substances imitate natural neuromediators and take their place on their receptors. Morphine, for example, binds to the receptors for endorphin (a natural "morphine" produced by the brain), while nicotine binds to the receptors for acetylcholine.
* Other substances increase the secretion of natural neuromediators. Cocaine, for example, mainly increases the amount of dopamine in the synapses, while ecstasy mainly increases the amount of serotonin.
* Still other substances block a natural neuromediator. Alcohol, for example, blocks the NMDA receptors.
Click on the names of each of the following drugs to read about how they work and what effects they have.
Alcohol ----- Opiates (heroin, morphine, etc.) ----- Cocaine ----- Nicotine
Caffeine ----- Amphetamines ----- Cannabis ----- Ecstasy ----- Benzodiazepines
Alcohol
Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.
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.
Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.
The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.
However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.
Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down.
Cannabis
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.
In chronic consumers of cannabis, the loss of CB1 receptors in the brain’s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.
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