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Updated: Aug 14, 2025
Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex
Published on: February 8, 2020
Schizophrenia risk-gene Crmp2 deficiency causes precocious critical period plasticity and deteriorated binocular
Yuan Zhang1, Li Yao1, Xiang Li1
1State Key Laboratory of Cognitive Neuroscience & Learning, IDG/McGovern Institute for Brain Research, Beijing Normal University, Beijing 100875, China.
Abstract:
Brain-specific loss of a microtubule-binding protein collapsin response mediator protein-2 (CRMP2) in the mouse recapitulates many schizophrenia-like behaviors of human patients, possibly resulting from associated developmental deficits in neuronal differentiation, path-finding, and synapse formation. However, it is still unclear how the Crmp2 loss affects neuronal circuit function and plasticity. By conducting in vivo and ex vivo electrophysiological recording in the mouse primary visual cortex (V1), we reveal that CRMP2 exerts a key regulation on the timing of postnatal critical period (CP) for experience-dependent circuit plasticity of sensory cortex. In the developing V1, the Crmp2 deficiency induces not only a delayed maturation of visual tuning functions but also a precocious CP for visual input-induced ocular dominance plasticity and its induction activity - coincident binocular inputs right after eye-opening. Mechanistically, the Crmp2 deficiency accelerates the maturation process of cortical inhibitory transmission and subsequently promotes an early emergence of balanced excitatory-inhibitory cortical circuits during the postnatal development. Moreover, the precocious CP plasticity results in deteriorated binocular depth perception in adulthood. Thus, these findings suggest that the Crmp2 deficiency dysregulates the timing of CP for experience-dependent refinement of circuit connections and further leads to impaired sensory perception in later life.
Insights
Collapsin response mediator protein-2 (CRMP2) loss in mice alters brain development, affecting critical periods for visual plasticity and leading to impaired depth perception. This suggests CRMP2 is crucial for normal sensory development and function.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Schizophrenia-like behaviors in mice are linked to brain-specific loss of CRMP2.
- CRMP2's role in neuronal differentiation, path-finding, and synapse formation is implicated.
- The precise impact of CRMP2 loss on neuronal circuit function and plasticity remains unclear.
Purpose of the Study:
- To investigate how CRMP2 deficiency affects neuronal circuit function and plasticity in the developing brain.
- To determine CRMP2's regulatory role in the timing of critical periods for sensory cortex plasticity.
- To elucidate the mechanisms underlying CRMP2's influence on visual circuit development and perception.
Main Methods:
- In vivo and ex vivo electrophysiological recordings in the mouse primary visual cortex (V1).
- Analysis of visual tuning functions and ocular dominance plasticity.
- Assessment of excitatory-inhibitory balance in cortical circuits during postnatal development.
Main Results:
- CRMP2 deficiency delays visual tuning maturation but causes a precocious critical period (CP) for ocular dominance plasticity.
- Accelerated maturation of cortical inhibitory transmission and early emergence of balanced excitatory-inhibitory circuits were observed.
- Precocious CP plasticity in CRMP2-deficient mice led to impaired binocular depth perception in adulthood.
Conclusions:
- CRMP2 is critical for regulating the timing of the postnatal critical period for experience-dependent sensory cortex plasticity.
- CRMP2 deficiency dysregulates CP timing, impacting circuit refinement and leading to sensory perception deficits.
- These findings highlight CRMP2's role in normal brain development and sensory processing.
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