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URPP Adaptive Brain Circuits in Development and Learning (AdaBD)

The impact of Cajal-Retzius cell death on the development of the cortical circuit

AdaBD made easy

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Certain brain cells are produced in large numbers during development and then have to be broken down again. What is the function of these cells? Does a disruption in the normal course of these events lead to deficits in sensory processing and learning?

In this project we discovered that death of certain brain cells  is essential for correct circuit development in the brain. A disruption in the normal course of events leads to delayed learning and reduced performance in a texture discrimination task in mice.  In future projects we plan to investigate if perturbations in the regulation of these temporary cells  are seen in known developmental disorders.

Research project

During prenatal development, Cajal Retzius cells (CRs) populate the outer-most layer of the developing mammalian neocortex (layer 1, L1). CRs have been shown to be synaptically integrated in the local circuit and to mainly receive inputs from GABAergic interneurons. Over the course of the first two postnatal weeks the number of CRs decreases. Utilizing anatomical, functional and behavioral approaches our project aims to reveal how the transient population of CRs contributes to building the mature neocortical somatosensory circuit and how their cell death assists in the proper formation and function of the circuit.

The project addresses the general question how the brain adapts its elements over the course of development for optimal sensory processing and how perturbation of the normal progression of transient developmental events can lead to deficits in sensory processing and learning.

Research groups

Principal investigators: Theofanis Karayannis, Fritjof Helmchen

PhD student: Angeliki Damilou

Publications

Damilou A, Cai L, Argunşah AÖ, Han S, Kanatouris G, Karatsoli M, Hanley O, Gesuita L, Kollmorgen S, Helmchen F, Karayannis T (2024)
Developmental Cajal-Retzius cell death contributes to the maturation of layer 1 cortical inhibition and somatosensory processing
Nature Communications 15, 6501