Two pathways, two kinds of symptoms
The dopamine hypothesis links the symptoms of schizophrenia to imbalanced dopamine signalling in different brain pathways. Excess dopamine activity in the mesolimbic pathway is associated with positive symptoms such as hallucinations and delusions, the experiences that are added to normal functioning. Reduced dopamine activity in the mesocortical pathway, projecting to the prefrontal cortex, is linked to negative symptoms such as blunted emotion, reduced motivation, and cognitive difficulty.
This dual picture helps explain a long-standing clinical puzzle: medications that block dopamine often ease positive symptoms while doing relatively little for negative ones, and can even worsen them by further lowering already low cortical dopamine.
Why the model is a partial explanation
The dopamine hypothesis is influential but incomplete. Other neurotransmitters, notably glutamate, along with genetic, developmental, and environmental factors, are now understood to contribute, and modern accounts treat dopamine as one important strand rather than the whole cause.
This is general educational information about a scientific model, not medical advice. Schizophrenia requires assessment and treatment by qualified mental health professionals.