ABSTRACT
Antipsychotic drugs (APDs) act on a variety of brain receptors and regions. Determining which ones are responsible for improving schizophrenia symptoms has been largely controversial. The prevalent view is that APD clinical efficacy seems to be related to their ability to block dopamine (DA) D2 receptors (1). Atypical antipsychotics are also D2 antagonists, but they differ from classical APDs on a number of aspects: a) they block serotonin 5-HT2 receptors with higher affinity than classical APDs (2,3), b) their D2 receptor occupancy is typically less than 80% at clinically effective doses (4), and c) they seem to have some selectivity in the brain regions they affect. Perhaps assessing the electrophysiological actions of APDs may bring clues to elucidate why they are effective and what makes atypical APDs different. This chapter will review the neurophysiolgical actions of this class of drugs, taking into consideration both acute and chronic effects.
