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Visual Cortical Plasticity: Molecular Mechanisms as Revealed by Induction Paradigms in Rodents

Journal

Publisher

MDPI
DOI: 10.3390/ijms24054701

Keywords

visual cortex; ocular-dominance plasticity; stimulus-selective response potentiation; cross-modal plasticity

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Assessing the molecular mechanism of synaptic plasticity in the cortex is crucial for identifying potential targets in conditions marked by defective plasticity. In this review, two major plasticity protocols (ocular-dominance and cross-modal) in rodents are discussed, focusing on the molecular signaling pathways involved. Additionally, the contribution of different populations of inhibitory and excitatory neurons at different time points is highlighted. The potentially disrupted molecular and circuit alterations in various neurodevelopmental disorders are also explored, and new plasticity paradigms, such as stimulus-selective response potentiation, are presented as potential tools to repair plasticity defects.
Assessing the molecular mechanism of synaptic plasticity in the cortex is vital for identifying potential targets in conditions marked by defective plasticity. In plasticity research, the visual cortex represents a target model for intense investigation, partly due to the availability of different in vivo plasticity-induction protocols. Here, we review two major protocols: ocular-dominance (OD) and cross-modal (CM) plasticity in rodents, highlighting the molecular signaling pathways involved. Each plasticity paradigm has also revealed the contribution of different populations of inhibitory and excitatory neurons at different time points. Since defective synaptic plasticity is common to various neurodevelopmental disorders, the potentially disrupted molecular and circuit alterations are discussed. Finally, new plasticity paradigms are presented, based on recent evidence. Stimulus-selective response potentiation (SRP) is one of the paradigms addressed. These options may provide answers to unsolved neurodevelopmental questions and offer tools to repair plasticity defects.

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