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Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
by
Kim, Daesoo
, Kim, Ryunhee
, Kim, Eunjoon
, Lee, Dongsoo
, Kang, Jaeseung
, Lee, Eunee
, Jung, Min Whan
, Lee, Jong Won
, Park, Hanwool
, Park, Sae-Geun
, Rhim, Issac
, Choi, Yeonsoo
, Lee, Seungjoon
, Park, Haram
, Choi, Jeonghoon
, Bae, Yong Chul
, Choi, Su Yeon
, Cho, Yi Sul
, Chung, Woosuk
, Kim, Myoung-Hwan
in
13/1
/ 13/51
/ 14/19
/ 14/35
/ 631/378/1457/1945
/ 631/378/1595/1554
/ 631/378/2591
/ 631/378/3919
/ 64/60
/ 9/30
/ 9/74
/ Animal Genetics and Genomics
/ Animals
/ Animals, Newborn
/ Autism
/ Behavioral Sciences
/ Biological Techniques
/ Biomedicine
/ Case-Control Studies
/ Cells, Cultured
/ Communication
/ Excitatory Amino Acid Antagonists - pharmacology
/ Excitatory Amino Acid Antagonists - therapeutic use
/ Exploratory Behavior - drug effects
/ Exploratory Behavior - physiology
/ Feeding Behavior - drug effects
/ Feeding Behavior - physiology
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - physiology
/ Grooming - drug effects
/ Grooming - physiology
/ Male
/ Medical research
/ Medicine, Experimental
/ Mice
/ Mice, Inbred C57BL
/ Mice, Transgenic
/ Mutation - genetics
/ Nerve Tissue Proteins - genetics
/ Neural transmission
/ Neurobiology
/ Neurons - drug effects
/ Neurons - physiology
/ Neurons - ultrastructure
/ Neurosciences
/ Pervasive developmental disorders
/ Physicists
/ Psychological aspects
/ Receptor, Metabotropic Glutamate 5 - metabolism
/ Receptors, N-Methyl-D-Aspartate - metabolism
/ Recognition (Psychology) - drug effects
/ Recognition (Psychology) - physiology
/ Schizophrenia
/ Social Behavior Disorders - drug therapy
/ Social Behavior Disorders - genetics
/ Social interaction
/ Socialization
/ Vocalization, Animal - drug effects
/ Vocalization, Animal - physiology
2015
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Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
by
Kim, Daesoo
, Kim, Ryunhee
, Kim, Eunjoon
, Lee, Dongsoo
, Kang, Jaeseung
, Lee, Eunee
, Jung, Min Whan
, Lee, Jong Won
, Park, Hanwool
, Park, Sae-Geun
, Rhim, Issac
, Choi, Yeonsoo
, Lee, Seungjoon
, Park, Haram
, Choi, Jeonghoon
, Bae, Yong Chul
, Choi, Su Yeon
, Cho, Yi Sul
, Chung, Woosuk
, Kim, Myoung-Hwan
in
13/1
/ 13/51
/ 14/19
/ 14/35
/ 631/378/1457/1945
/ 631/378/1595/1554
/ 631/378/2591
/ 631/378/3919
/ 64/60
/ 9/30
/ 9/74
/ Animal Genetics and Genomics
/ Animals
/ Animals, Newborn
/ Autism
/ Behavioral Sciences
/ Biological Techniques
/ Biomedicine
/ Case-Control Studies
/ Cells, Cultured
/ Communication
/ Excitatory Amino Acid Antagonists - pharmacology
/ Excitatory Amino Acid Antagonists - therapeutic use
/ Exploratory Behavior - drug effects
/ Exploratory Behavior - physiology
/ Feeding Behavior - drug effects
/ Feeding Behavior - physiology
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - physiology
/ Grooming - drug effects
/ Grooming - physiology
/ Male
/ Medical research
/ Medicine, Experimental
/ Mice
/ Mice, Inbred C57BL
/ Mice, Transgenic
/ Mutation - genetics
/ Nerve Tissue Proteins - genetics
/ Neural transmission
/ Neurobiology
/ Neurons - drug effects
/ Neurons - physiology
/ Neurons - ultrastructure
/ Neurosciences
/ Pervasive developmental disorders
/ Physicists
/ Psychological aspects
/ Receptor, Metabotropic Glutamate 5 - metabolism
/ Receptors, N-Methyl-D-Aspartate - metabolism
/ Recognition (Psychology) - drug effects
/ Recognition (Psychology) - physiology
/ Schizophrenia
/ Social Behavior Disorders - drug therapy
/ Social Behavior Disorders - genetics
/ Social interaction
/ Socialization
/ Vocalization, Animal - drug effects
/ Vocalization, Animal - physiology
2015
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Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
by
Kim, Daesoo
, Kim, Ryunhee
, Kim, Eunjoon
, Lee, Dongsoo
, Kang, Jaeseung
, Lee, Eunee
, Jung, Min Whan
, Lee, Jong Won
, Park, Hanwool
, Park, Sae-Geun
, Rhim, Issac
, Choi, Yeonsoo
, Lee, Seungjoon
, Park, Haram
, Choi, Jeonghoon
, Bae, Yong Chul
, Choi, Su Yeon
, Cho, Yi Sul
, Chung, Woosuk
, Kim, Myoung-Hwan
in
13/1
/ 13/51
/ 14/19
/ 14/35
/ 631/378/1457/1945
/ 631/378/1595/1554
/ 631/378/2591
/ 631/378/3919
/ 64/60
/ 9/30
/ 9/74
/ Animal Genetics and Genomics
/ Animals
/ Animals, Newborn
/ Autism
/ Behavioral Sciences
/ Biological Techniques
/ Biomedicine
/ Case-Control Studies
/ Cells, Cultured
/ Communication
/ Excitatory Amino Acid Antagonists - pharmacology
/ Excitatory Amino Acid Antagonists - therapeutic use
/ Exploratory Behavior - drug effects
/ Exploratory Behavior - physiology
/ Feeding Behavior - drug effects
/ Feeding Behavior - physiology
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - physiology
/ Grooming - drug effects
/ Grooming - physiology
/ Male
/ Medical research
/ Medicine, Experimental
/ Mice
/ Mice, Inbred C57BL
/ Mice, Transgenic
/ Mutation - genetics
/ Nerve Tissue Proteins - genetics
/ Neural transmission
/ Neurobiology
/ Neurons - drug effects
/ Neurons - physiology
/ Neurons - ultrastructure
/ Neurosciences
/ Pervasive developmental disorders
/ Physicists
/ Psychological aspects
/ Receptor, Metabotropic Glutamate 5 - metabolism
/ Receptors, N-Methyl-D-Aspartate - metabolism
/ Recognition (Psychology) - drug effects
/ Recognition (Psychology) - physiology
/ Schizophrenia
/ Social Behavior Disorders - drug therapy
/ Social Behavior Disorders - genetics
/ Social interaction
/ Socialization
/ Vocalization, Animal - drug effects
/ Vocalization, Animal - physiology
2015
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Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
Journal Article
Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
2015
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Overview
Enhanced NMDA receptor function and social interaction deficits are observed in mice lacking the excitatory postsynaptic scaffolding protein IRSp53. Reducing NMDAR activity by pharmacological methods rescues the impaired social interaction observed in these mice. This suggests that enhanced NMDA receptor function may be associated with social deficits.
Social deficits are observed in diverse psychiatric disorders, including autism spectrum disorders and schizophrenia. We found that mice lacking the excitatory synaptic signaling scaffold IRSp53 (also known as BAIAP2) showed impaired social interaction and communication. Treatment of
IRSp53
−/−
mice, which display enhanced NMDA receptor (NMDAR) function in the hippocampus, with memantine, an NMDAR antagonist, or MPEP, a metabotropic glutamate receptor 5 antagonist that indirectly inhibits NMDAR function, normalized social interaction. This social rescue was accompanied by normalization of NMDAR function and plasticity in the hippocampus and neuronal firing in the medial prefrontal cortex. These results, together with the reduced NMDAR function implicated in social impairments, suggest that deviation of NMDAR function in either direction leads to social deficits and that correcting the deviation has beneficial effects.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 13/51
/ 14/19
/ 14/35
/ 64/60
/ 9/30
/ 9/74
/ Animal Genetics and Genomics
/ Animals
/ Autism
/ Excitatory Amino Acid Antagonists - pharmacology
/ Excitatory Amino Acid Antagonists - therapeutic use
/ Exploratory Behavior - drug effects
/ Exploratory Behavior - physiology
/ Feeding Behavior - drug effects
/ Feeding Behavior - physiology
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - physiology
/ Male
/ Mice
/ Nerve Tissue Proteins - genetics
/ Pervasive developmental disorders
/ Receptor, Metabotropic Glutamate 5 - metabolism
/ Receptors, N-Methyl-D-Aspartate - metabolism
/ Recognition (Psychology) - drug effects
/ Recognition (Psychology) - physiology
/ Social Behavior Disorders - drug therapy
/ Social Behavior Disorders - genetics
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