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Visual Sequences Drive Experience-Dependent Plasticity in Mouse Anterior Cingulate Cortex.

Michael S Sidorov¹, Hyojin Kim², Marie Rougie²

¹Department of Cell Biology & Physiology, University of North Carolina, Chapel Hill, NC 27599, USA; Carolina Institute for Developmental Disabilities, University of North Carolina, Chapel Hill, NC 27599, USA; Neuroscience Center, University of North Carolina, Chapel Hill, NC 27599, USA; Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010, USA; Departments of Pediatrics and Pharmacology & Physiology, The George Washington University School of Medicine and Health Sciences, Washington, DC 20052, USA.

|September 16, 2020

Summary

This summary is machine-generated.

The anterior cingulate cortex (ACC) exhibits sequence plasticity, altering response timing rather than magnitude. This plasticity is impaired in a neurodevelopmental disorder model, highlighting functional differences between ACC and primary visual cortex (V1) in processing familiar visual sequences.

Keywords:

Angelman syndrome anterior cingulate plasticity visual cortex visually evoked potential

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Area of Science:

Neuroscience
Systems Neuroscience
Cognitive Neuroscience

Background:

Experience-dependent plasticity, particularly sequence plasticity, is well-understood in mouse primary visual cortex (V1).
The anterior cingulate cortex (ACC), a prefrontal region, responds to visual stimuli, but how its circuits are modified by visual experience remains largely unknown.

Purpose of the Study:

To investigate whether the ACC exhibits sequence plasticity.
To compare the characteristics of sequence plasticity in the ACC with those in the V1.
To examine the impact of a neurodevelopmental disorder on ACC sequence plasticity.

Main Methods:

Utilized electrophysiological recordings in mouse ACC and V1.
Presented familiar visual sequences to assess experience-dependent changes in neural responses.
Investigated sequence plasticity in both wild-type and a mouse model of a neurodevelopmental disorder.

Main Results:

Mouse ACC demonstrates sequence plasticity, characterized by altered response timing, unlike V1's magnitude changes.
Sequence plasticity was absent in the ACC of mice with the neurodevelopmental disorder, while V1 plasticity remained intact.
These findings reveal distinct mechanisms of familiarity encoding in ACC and V1.

Conclusions:

Simple sensory stimuli can reveal functional modifications in higher-order prefrontal circuits.
The ACC and V1 exhibit divergent strategies for encoding familiarity through experience-dependent plasticity.
Impaired sequence plasticity in the ACC may contribute to the cognitive deficits observed in neurodevelopmental disorders.