Schizophrenia is a complex neuropsychiatric disorder marked by a wide spectrum of symptoms, yet its biochemical basis remains unclear. While the classical dopamine hypothesis links excess dopaminergic activity to hallucinations and delusions, recent research implicates glutamatergic, GABAergic, serotonergic, and cholinergic systems, along with inflammatory and oxidative stress pathways. This paper argues that schizophrenia results from interactions among multiple neurotransmitter and receptor systems. By reviewing neuroimaging, pharmacological, and clinical trial evidence, it demonstrates that understanding receptor-specific contributions is crucial for developing targeted therapies addressing both cognitive deficits and affective symptoms.