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Specific disruption of thalamic inputs to the auditory cortex in schizophrenia models
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Specific disruption of thalamic inputs to the auditory cortex in schizophrenia models
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Journal Article
Specific disruption of thalamic inputs to the auditory cortex in schizophrenia models
2014
Overview
Auditory hallucinations in schizophrenia are alleviated by antipsychotic agents that inhibit D2 dopamine receptors (Drd2s). The defective neural circuits and mechanisms of their sensitivity to antipsychotics are unknown. We identified a specific disruption of synaptic transmission at thalamocortical glutamatergic projections in the auditory cortex in murine models of schizophrenia-associated 22q11 deletion syndrome (22q11DS). This deficit is caused by an aberrant elevation of Drd2 in the thalamus, which renders 22q11DS thalamocortical projections sensitive to antipsychotics and causes a deficient acoustic startle response similar to that observed in schizophrenic patients. Haploinsufficiency of the microRNA-processing gene Dgcr8 is responsible for the Drd2 elevation and hypersensitivity of auditory thalamocortical projections to antipsychotics. This suggests that Dgcr8-microRNA-Drd2–dependent thalamocortical disruption is a pathogenic event underlying schizophrenia-associated psychosis.
Publisher
American Association for the Advancement of Science,The American Association for the Advancement of Science
Subject
22q11 Deletion Syndrome - drug therapy
/ 22q11 Deletion Syndrome - genetics
/ Alleles
/ Animals
/ Antipsychotic Agents - therapeutic use
/ Auditory Cortex - metabolism
/ Axons
/ brain
/ cortex
/ genes
/ Mice
/ microRNA
/ Neurons
/ Receptors, Dopamine D2 - biosynthesis
/ Receptors, Dopamine D2 - genetics
/ RNA-Binding Proteins - genetics
/ Rodents
/ Schizophrenia - drug therapy
/ synapse
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