Antipsychotics block D2 receptors which reduces the amount of DA released into the synapse
The dopamine hypothesis is supported by evidence as it explains why antipsychotic drugs work.
Dopamine hypothesis is supported by evidence as antipsychotic drugs are effective at treating schizophrenia.
The dopamine hypothesis has been criticised because it doesn't explain all aspects of schizophrenia such as cognitive deficit and social withdrawal.
Cognitive deficit - difficulty concentrating or remembering things
However, there are limitations to the dopamine hypothesis such as not all schizophrenia patients respond well to antipsychotics and some people who don't have schizophrenia also experience high levels of DA.
Therefore, other theories suggest that glutamate may be involved in schizophrenia rather than just DA.
Glutamate is an excitatory neurotransmitter that stimulates neurons to fire action potentials.
However, there are limitations to the dopamine hypothesis such as not all people respond well to antipsychotic medication.
There are also other neurotransmitters involved in schizophrenia such as glutamate and GABA.
Glutamate is thought to be overactive in schizophrenia leading to too many connections between neurons (hyperconnectivity). This can lead to excessive stimulation of the brain causing hallucinations and delusions.
Social withdrawal - lack of interest in other people
Serotonin (5HT) is involved in mood regulation and low levels have been linked to depression.
There are alternative theories that suggest different neurotransmitters may be involved in schizophrenia such as serotonin and glutamate.
Some people with schizophrenia do not show increased activity in the mesolimbic pathway.
Dopamine receptor blockers (antipsychotics) only reduce positive symptoms of schizophrenia, leaving negative symptoms unchanged.