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Complete Disruption of the Kainate Receptor Gene Family Results in Corticostriatal Dysfunction in Mice.

Cell Rep. 2017 Feb 21;18(8):1848-1857
Jian Xu 1 , John J Marshall 1 , Herman B Fernandes 1 , Toshihiro Nomura 1 , Bryan A Copits 2 , Daniele Procissi 3 , Susumu Mori 4 , Lei Wang 5 , Yongling Zhu 6 , Geoffrey T Swanson 2 , Anis Contractor 7
Jian Xu 1 , John J Marshall 1 , Herman B Fernandes 1 , Toshihiro Nomura 1 , Bryan A Copits 2 , Daniele Procissi 3 , Susumu Mori 4 , Lei Wang 5 , Yongling Zhu 6 , Geoffrey T Swanson 2 , Anis Contractor 7
+ et al

[No authors listed]

Author information
  • 1 Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
  • 2 Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
  • 3 Department of Radiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
  • 4 Department of Radiology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
  • 5 Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
  • 6 Department of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
  • 7 Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA; Department of Neurobiology, Weinberg College of Arts and Sciences, Northwestern University, Evanston, IL 60208, USA. Electronic address: a-contractor@northwestern.edu.

摘要

Kainate receptors are members of the glutamate receptor family that regulate synaptic function in the brain. They modulate synaptic transmission and the excitability of neurons; however, their contributions to neural circuits that underlie behavior are unclear. To understand the net impact of kainate receptor signaling, we generated knockout mice in which all five kainate receptor subunits were ablated (5ko). These mice displayed compulsive and perseverative behaviors, including over-grooming, as well as motor problems, indicative of alterations in striatal circuits. There were deficits in corticostriatal input to spiny projection neurons (SPNs) in the dorsal striatum and correlated reductions in spine density. The behavioral alterations were not present in mice only lacking the primary receptor subunit expressed in adult striatum (GluK2 KO), suggesting that signaling through multiple receptor types is required for proper striatal function. This demonstrates that alterations in striatal function dominate the behavioral phenotype in mice without kainate receptors.

KEYWORDS: corticostriatal synapse, kainate receptor, perseverative behavior, striatum

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