Parvalbumin cell ablation of NMDA-R1 causes increased resting network excitability with associated social and self-care deficits

NMDA-receptor (NMDAR) hypofunction is strongly implicated in the pathophysiology of schizophrenia. Several convergent lines of evidence suggest that net excitation propagated by impaired NMDAR signaling on GABAergic interneurons may be of particular interest in mediating several aspects of schizophr...

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Veröffentlicht in:	Neuropsychopharmacology (New York, N.Y.) N.Y.), 2014-06, Vol.39 (7), p.1603-1613
Hauptverfasser:	Billingslea, Eddie N, Tatard-Leitman, Valerie M, Anguiano, Jaynie, Jutzeler, Catherine R, Suh, Jimmy, Saunders, John A, Morita, Susumu, Featherstone, Robert E, Ortinski, Pavel I, Gandal, Michael J, Lin, Robert, Liang, Yuling, Gur, Raquel E, Carlson, Gregory C, Hahn, Chang-Gyu, Siegel, Steven J
Format:	Artikel
Sprache:	eng
Schlagworte:	Ablation Animal cognition Animals Baclofen - pharmacology Behavior Brain - pathology Disease Models, Animal Evoked Potentials - drug effects Evoked Potentials - genetics Excitatory Amino Acid Antagonists - pharmacology Exploratory Behavior - physiology GABA Agonists - pharmacology Interpersonal Relations Kinases Laboratory animals Maze Learning - drug effects Mice Mice, Inbred C57BL Mice, Transgenic Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Neurons - drug effects Neurons - metabolism Original Parvalbumins - deficiency Parvalbumins - genetics Pathophysiology Pyridines - pharmacology Receptors, N-Methyl-D-Aspartate - genetics Receptors, N-Methyl-D-Aspartate - metabolism Rest Schizophrenia Self Care Social Behavior Disorders - genetics Social Behavior Disorders - pathology
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