Ketamine Administration During the Second Postnatal Week Alters Synaptic Properties of Fast-Spiking Interneurons in the Medial Prefrontal Cortex of Adult Mice

Cerebral Cortex
Vivek Jeevakumar, S Kroener

Abstract

The N-methyl-D-aspartic acid (NMDA)-hypofunction theory of schizophrenia suggests that schizophrenia is associated with a loss of NMDA receptors, specifically on corticolimbic parvalbumin (PV)-expressing GABAergic interneurons, leading to disinhibition of pyramidal cells and cortical desynchronization. However, the presumed changes in glutamatergic inputs onto PV interneurons have not been tested directly. We treated mice with the NMDAR antagonist ketamine during the second postnatal week and investigated persistent cellular changes in the adult medial prefrontal cortex (mPFC) using whole-cell patch-clamp recordings and immunohistochemistry. Parvalbumin expression in the mPFC was reduced in ketamine-treated (KET) mice, and γ-aminobutyric acid release onto pyramidal cells was reduced in layers 2/3, but not layer 5. Consistent with pyramidal cell disinhibition the frequency of spontaneous glutamatergic inputs onto PV cells was also increased in KET mice. Furthermore, developmental ketamine treatment resulted in an increased NMDA:AMPA ratio in evoked synaptic currents and larger amplitudes of spontaneous NMDAR currents, indicating a homeostatic upregulation of NMDARs in PV interneurons. This upregulation was specific to NR2B subun...Continue Reading

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NR2A NMDA receptor
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