The dopamine hypothesis

1. The dopamine hypothesis is the biological explanation of schizophrenia, and it ties the condition to one neurotransmitter.
2. Its central claim is that the dopamine system is overactive, producing high dopamine levels in the brain.
3. That excess activity is linked most strongly to the positive symptoms, such as hallucinations and delusions.
4. The explanation covers the neurons involved, how they pass a signal, and what happens when the system is overactive.

Dopaminergic neurons

1. Dopaminergic neurons are the brain cells that use dopamine as their chemical messenger.
2. Like any neuron, each one has a cell body, branching dendrites that receive signals, and a long axon that carries a signal away.
3. Dopamine is made inside the neuron and stored in tiny sacs called vesicles at the end of the axon.
4. These neurons run in pathways deep inside the brain, and those pathways are involved in movement, motivation and deciding what deserves attention.

Synaptic transmission

1. An electrical impulse travels down the axon of the sending neuron to the axon terminal.
2. The impulse pushes the vesicles against the membrane and they burst open.
3. Dopamine spills into the synapse, the microscopic gap between the two neurons.
4. It diffuses across, so this part of the message is chemical.
5. On the other side it binds to receptors on the dendrites of the receiving neuron, and only a receptor of the matching shape will accept it.
6. Once enough receptors are occupied, the receiving neuron fires its own impulse.
7. Whatever dopamine is left in the gap gets cleared away, either broken down by enzymes or pulled back into the sending neuron by reuptake.
8. Clearing the gap is what stops the signal, so both the amount of dopamine and how long it lingers there matter.

How the system becomes overactive

1. In schizophrenia the dopaminergic neurons are thought to fire more often than they should.
2. Each extra firing releases more dopamine into the synapse.
3. Some brains also appear to have more dopamine receptors, so the same amount of dopamine produces more binding.
4. If reuptake is slower, dopamine sits in the gap for longer and keeps stimulating the receiving neuron.
5. Together these produce high dopamine activity, with receiving neurons firing when nothing real has triggered them.
6. In the pathways that handle sound and speech, that misfiring is experienced as a voice, which is an auditory hallucination.
7. Dopamine also flags what is important, so too much of it makes ordinary events feel loaded with meaning.
   1. A car parked outside starts to feel like surveillance, and the belief that grows around that feeling becomes a delusion.

Evidence for the dopamine hypothesis

1. Drugs that raise dopamine activity, such as amphetamines and cocaine, can produce hallucinations and delusions in people who have never had schizophrenia.
2. The same drugs can make existing symptoms worse in a person who has been diagnosed.
3. L-dopa, given to raise dopamine in Parkinson's disease, can produce similar symptoms as a side effect.
4. Anti-psychotic drugs block dopamine receptors so that less binding takes place, and they reduce the positive symptoms.
   1. The more strongly a drug blocks dopamine receptors, the better it tends to work on those symptoms.
5. In Daniel et al. (1991), amphetamine given to ten in-patients raised activity in the prefrontal area and improved their scores on a card sorting task.
   1. That supports the theory by showing dopamine activity and thinking move together.

Turning this into marks

1. When two parts of the explanation are asked for, make them genuinely separate rather than one part rephrased.
2. Name dopamine, the dopaminergic neuron and the synapse, because a general reference to brain chemistry does not secure the knowledge mark.
3. The mark most often lost is describing the symptoms without saying what happens at the synapse.