NORMAL DOPAMINE FUNCTION
The gap where an electrical signal jumps from one neuron to another is called the synaptic cleft. This is a closeup of the cleft between one neuron and another. Since the impulse cannot cross a gap as electricity, it crosses as a chemical message by means of \"messengers\" called neurotransmitters. One important neurotransmitter involved in the experience of pleasure is called dopamine.
Here, dopamine, shown in yellow, is produced in the neuron shown at the top and packaged in containers called vesicles. As an electrical impulse arrives at the neuron\'s terminal, the vesicle moves to the neural membrane and releases its load of dopamine into the synaptic cleft.
The dopamine crosses the gap and binds to receiver sites, or receptors, on the membrane of the next neuron. When dopamine occupies a receptor, various actions take place in that neuron: certain ions, shown in green, exit or enter, and certain enzymes are released or inhibited. The result is that a new electrical impulse is generated in this neuron, and the \"message\" continues on.
After the dopamine has bound to the receptor, eventually it comes off again and is removed fom the synaptic cleft and back into the first neuron by reuptake pumps. (For normal nerve transmission, it is important that the dopamine not stay in the cleft.)

WHEN COCAINE IS ADDED
This is what happens to nerve cell transmission when cocaine, shown in red, enters the brain\'s reward pathway. Cocaine blocks the reuptake pumps which act to remove dopamine from the synapse. More dopamine accumulates in the synapse, resulting in feelings of intense pleasure.
Unfortunately, prolonged cocaine use may cause the brain to adapt, such that it comes to depend on the presence of cocaine to function normally, \"downregulating\" the amount of dopamine present naturally.
Then, if the person stops using cocaine, there is not enough dopamine in the synapses, and the person experiences the opposite of pleasure--depression, fatigue, and low mood. The immediate, worst symptoms are called withdrawal.
Even long after the person has stopped using cocaine, brain abnormalities can persist, causing feelings of discomfort and craving for more of the drug to relieve these feelings.


NORMAL GABA FUNCTION
The gap where an electrical signal jumps from one neuron to another is called the synaptic cleft. This is a closeup of the cleft between one neuron and another. Since the impulse cannot cross a gap as electricity, it crosses as a \"message\" by means of chemical messengers called neurotransmitters.
This animation shows the action of a neurotransmitter called GABA, which acts to quiet electrical activity in parts of the brain. The GABA is produced in one neuron, here the one shown at the top. It is stored in packages called vesicles that move to the cell membrane and release the GABA into the cleft. The GABA crosses the gap between the neurons, and then binds to receiver sites, or receptors, on the neighboring neuron, shown at the bottom.
When GABA occupies a receptor, it decreases the neuron\'s electrical activity. (That is, the neuron\'s electrical activity \"quiets down.\") After a while, the GABA comes off the receptor and is removed from the synapse by reuptake pumps that return it to the first neuron.

WHEN ALCOHOL IS ADDED
When GABA binds to its receptors, channels in the neuron flicker open and closed, allowing negatively charged molecules called ions (shown here in white) to move into the neuron. This decreases the neuron\'s activity.
This close-up shows the opening of the ion channels in normal GABA binding, and then when alcohol is added.
Alcohol, shown in black, also binds to the GABA receptors, and increases the quieting effect that GABA has on neurons. Researchers are not sure exactly how it does so, but one theory holds that it causes the ion channels to stay open longer, thus increasing the ion flow. The result is a much greater quieting effect on the brain.
Because there are GABA receptors in many parts of the brain, many different parts are affected. This accounts for alcohol\'s sedating effect on many functions controlled by the brain--judgment, movement, and even breathing.
Unfortunately, prolonged alcohol use may cause the brain to adapt, so it comes to depend on the presence of alcohol to function normally. Then, if the person stops drinking, he or she experiences anxiety, jitteriness, emotional discomfort, insomnia, possibly tremors, and, in severe alcoholism, sometimes convulsions and/or death.
Even long after the person has stopped drinking alcohol, brain abnormalities can persist, causing feelings of discomfort and craving for more alcohol to relieve these feelings.


NORMAL DOPAMINE FUNCTION
The gap where an electrical signal jumps from one neuron to another is called the synaptic cleft. This is a closeup of the cleft between one neuron and another. Since the impulse cannot cross a gap as electricity, it crosses as a message by means of chemical \"messengers\" called neurotransmitters. One important neurotransmitter involved in the experience of pleasure is called dopamine.
Here, dopamine, shown in yellow, is produced in the neuron shown at the top and packaged in containers called vesicles. As an electrical impulse arrives at the neuron\'s terminal, the vesicle moves to the neural membrane and releases its load of dopamine into the synaptic cleft. The dopamine crosses the gap and binds to receiver sites, or receptors, on the membrane of the next neuron. When dopamine occupies a receptor, various actions take place in that neuron so that a new electrical impulse is generated in this neuron, and the \"message\" continues on.
After the dopamine has bound to the receptor, eventually it comes off again and is removed fom the synaptic cleft and back into the first neuron by reuptake pumps. (For normal nerve transmission, it is important that the dopamine not stay in the cleft.)

WHEN OPIATES ARE ADDED
This animation shows what happens to dopamine transmission when an opiate drug such as heroin or morphine enters the brain\'s reward pathway.
The opiate, shown in red, binds to opiate receptors on another neuron, shown here at the right. (The reason that some neurons have special receptors for opiates is probably that there are naturally occuring opiates in the brain.)
This causes the amount of dopamine in the synaptic clefts in the reward pathway to increase dramatically, as shown in the close-up of the synaptic cleft to the left.
Researchers are still not sure exactly how opiate drugs cause this increase in dopamine, but one theory says that when the opiate binds to the receptors on the third neuron shown, that neuron releases less GABA, which is a neurotransmitter that inhibits dopamine. (If there is less GABA, therefore, there is more dopamine.)
The increase in dopamine results in feelings of intense pleasure for the person taking the opiate drug.
Unfortunately, prolonged opiate use may cause the brain to adapt, so it comes to depend on the presence of the drug just to function normally. Then, if the person stops using the drug, he or she experiences the opposite of pleasure--anxiety, irritability, and low mood. The immediate, worst symptoms are called withdrawal.
Opiate withdrawal has physical symptoms as well as psychological ones; these include nausea, chills, cramps, and sweating.
Even long after the person has stopped using opiates, brain abnormalities can persist, causing feelings of discomfort and craving for more of the drug to relieve these feelings.

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