Structural and functional differences in the barrel cortex of Mecp2 null mice.

Area of Science:

• Neuroscience
• Developmental Biology
• Genetics

Background:

• Sensory system functional deficits are common in neurodevelopmental disorders like Rett syndrome (RTT).
• Mutations in the methyl CpG binding protein 2 (MECP2) gene are the primary cause of RTT.
• Mouse models with Mecp2 gene alterations offer insights into RTT-related brain development.

Purpose of the Study:

• To investigate the somatosensory cortical phenotype in the Bird mouse model of RTT.
• To evaluate whisker sensory evoked activity and barrel cortex structure in Mecp2-deficient mice.

Main Methods:

• Voltage-sensitive dye imaging to assess whisker sensory evoked activity in the barrel cortex.
• Morphological analyses of dendritic differentiation in barrel neurons and thalamocortical axon (TCA) arbors.
• Study conducted on postnatal mice, including Mecp2-deficient males.

Main Results:

• Whisker-evoked activity in the barrel cortex of Mecp2-deficient mice was topographic but weak.
• TCA arbors did not form discrete patches in barrel hollows.
• Dendritic branch complexity in layer IV spiny stellate neurons was reduced.

Conclusions:

• Mecp2 deficiency causes significant structural and functional impairments in the barrel cortex of the Bird mouse model.
• These anomalies may underlie tactile sensitivity deficits and sensorimotor stereotypies observed in RTT.
• The findings highlight the role of MECP2 in the proper development of the primary somatosensory cortex.