Dopamine hypothesis has dominated as a molecular pathology of schizophrenia over the past few decades and anti-dopaminergic drugs are currently the most widespread available treatment option. Converging lines of evidence suggest altered regulation of other neurotransmitters including glutamate, GABA and acetylcholine, results in the dysregulation of dopaminergic neurons in schizophrenia, and is involved in the comprehensive symptoms such as positive, negative, and cognitive dysfunction. In the prefrontal cortex of patients with schizophrenia; dysfunctional NMDA-type glutamate receptors on GABAergic interneurons cause disinhibition of pyramidal glutamatergic neurons, resulting in increase in the firing of dopaminergic neurons. Cognitive dysfunction of schizophrenia may be a representation of asynchronous glutamatergic and GABAergic neurons. In addition to the effects of NMDA receptor modulators including D-serine, emerging evidences of the roles of nicotinic acetylcholine receptors on glutamatergic and dopaminergic regulations suggest new treatment options for schizophrenia.