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Evaluation of Hemisphere Lateralization with Bilateral Local Field Potential Recording in Secondary Motor Cortex of Mice

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Gamma rhythms link prefrontal interneuron dysfunction with cognitive inflexibility in Dlx5/6(+/-) mice.

Kathleen K A Cho¹, Renee Hoch², Anthony T Lee¹

¹Department of Psychiatry, University of California, San Francisco, San Francisco, CA 94143, USA; Center for Integrative Neuroscience, University of California, San Francisco, San Francisco, CA 94143, USA; Sloan-Swartz Center for Theoretical Neurobiology, University of California, San Francisco, San Francisco, CA 94143, USA.

|March 11, 2015

Summary

Abnormalities in fast-spiking interneurons (FSINs) disrupt cognitive function in schizophrenia. Restoring gamma oscillations in the prefrontal cortex (PFC) can reverse cognitive inflexibility, suggesting a therapeutic target.

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Area of Science:

Neuroscience
Psychiatry
Genetics

Background:

Schizophrenia is linked to abnormalities in GABAergic interneurons and disrupted gamma (γ) oscillations in the prefrontal cortex (PFC).
The precise role of γ rhythms in PFC-dependent cognition and the mechanisms behind schizophrenia's post-adolescent onset remain unclear.

Purpose of the Study:

To investigate the causal link between fast-spiking interneuron (FSIN) dysfunction, γ oscillations, and cognitive deficits in a mouse model of schizophrenia.
To explore the potential of modulating PFC γ oscillations as a therapeutic strategy for schizophrenia endophenotypes.

Main Methods:

Utilized mice heterozygous for Dlx5/6, which exhibit abnormal GABAergic interneuron development.
Assessed cognitive flexibility and task-evoked γ oscillations in Dlx5/6(+/-) mice before and after adolescence.
Manipulated PFC interneuron activity using inhibition and frequency-specific stimulation in control and Dlx5/6(+/-) mice.

Main Results:

Dlx5/6(+/-) mice showed FSIN abnormalities post-adolescence, coinciding with cognitive inflexibility and reduced task-evoked γ oscillations.
Inhibiting PFC interneurons in control mice mimicked the cognitive deficits observed in Dlx5/6(+/-) mice.
Frequency-specific γ-frequency stimulation of PFC interneurons restored cognitive flexibility in adult Dlx5/6(+/-) mice, with persistent effects.

Conclusions:

Abnormal FSIN development contributes to the post-adolescent onset of schizophrenia-like cognitive endophenotypes.
PFC interneuron-driven γ oscillations play a causal role in cognitive flexibility, offering a potential therapeutic target for schizophrenia.