Specific disruption of thalamic inputs to the auditory cortex in schizophrenia models

Abstract

Genes, synapses, and hallucinations In a schizophrenia mouse model, Chun et al. found that an abnormal increase of dopamine D2 receptors in the brain's thalamic nuclei caused thalamocortical synapse deficits owing to reduced glutamate release. Antipsychotic agents or a dopamine receptor antagonist reversed this down-regulation. The defect was associated with the loss of a component of the microRNA processing machinery encoded by the dgcr8 gene. Science , this issue p. 1178