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Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
Published on: May 12, 2015
Brain-specific Crmp2 deletion leads to neuronal development deficits and behavioural impairments in mice
Hongsheng Zhang1, Eunchai Kang2,3, Yaqing Wang1
1State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
Abstract:
Several genome- and proteome-wide studies have associated transcription and translation changes of CRMP2 (collapsing response mediator protein 2) with psychiatric disorders, yet little is known about its function in the developing or adult mammalian brain in vivo. Here we show that brain-specific Crmp2 knockout (cKO) mice display molecular, cellular, structural and behavioural deficits, many of which are reminiscent of neural features and symptoms associated with schizophrenia. cKO mice exhibit enlarged ventricles and impaired social behaviour, locomotor activity, and learning and memory. Loss of Crmp2 in the hippocampus leads to reduced long-term potentiation, abnormal NMDA receptor composition, aberrant dendrite development and defective synapse formation in CA1 neurons. Furthermore, knockdown of crmp2 specifically in newborn neurons results in stage-dependent defects in their development during adult hippocampal neurogenesis. Our findings reveal a critical role for CRMP2 in neuronal plasticity, neural function and behavioural modulation in mice.
Insights
Collapsing response mediator protein 2 (CRMP2) is crucial for brain development and function. Loss of CRMP2 in mice leads to molecular, cellular, and behavioral deficits, impacting neuronal plasticity and potentially schizophrenia-related symptoms.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Genome-wide studies link CRMP2 (collapsing response mediator protein 2) alterations to psychiatric disorders.
- The in vivo function of CRMP2 in the developing and adult mammalian brain remains largely unknown.
Purpose of the Study:
- To investigate the role of CRMP2 in the mammalian brain using a conditional knockout mouse model.
- To elucidate the molecular, cellular, structural, and behavioral consequences of CRMP2 loss in vivo.
Main Methods:
- Generation of brain-specific Crmp2 knockout (cKO) mice.
- Assessment of molecular, cellular, structural, and behavioral phenotypes.
- Electrophysiological recordings (long-term potentiation) in hippocampal CA1 neurons.
- Analysis of NMDA receptor composition and dendritic morphology.
- CRMP2 knockdown in adult hippocampal neurogenesis.
Main Results:
- cKO mice exhibited enlarged ventricles, impaired social behavior, locomotor activity, learning, and memory.
- Hippocampal CRMP2 loss reduced long-term potentiation, altered NMDA receptor composition, and impaired dendrite and synapse formation.
- Knockdown of CRMP2 in newborn neurons caused stage-dependent developmental defects during adult neurogenesis.
Conclusions:
- CRMP2 plays a critical role in neuronal plasticity, neural function, and behavioral modulation in mice.
- CRMP2 deficits may contribute to neurodevelopmental and psychiatric conditions like schizophrenia.
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