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Cerebellar structure and function abnormalities in 16p11.2 microduplication mice.

Cessily Hayes^1,2,3, Hunter Halverson^1,2, Krisha Keeran¹

¹Iowa Neuroscience Institute, University of Iowa, Iowa City, IA 52242, USA.

Brain Communications

|May 18, 2026

Summary

This summary is machine-generated.

16p11.2 microduplication in mice shows specific cerebellar lobule VI abnormalities, impacting associative learning. These findings may illuminate the cerebellar role in neuropsychiatric disorders like schizophrenia.

Keywords:

Purkinje cells cerebellar learning cerebellum eyeblink conditioning stellate cells

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Area of Science:

Neuroscience
Genetics
Developmental Biology

Background:

16p11.2 microduplication is linked to neuropsychiatric disorders, with cerebellar abnormalities implicated.
Previous studies show cerebellar transcriptional dysregulation and reduced volume in 16p11.2 duplication models.

Purpose of the Study:

To characterize cerebellar anatomy and function in 16p11.2 microduplication (16p11.2^dp/+) mice.
To investigate the impact of 16p11.2 microduplication on cerebellar-dependent learning.

Main Methods:

Histological examination of the cerebellar cortex in 16p11.2^dp/+ mice.
Assessment of gait, motor coordination, and delay eyeblink conditioning.

Main Results:

No structural differences or motor impairments were found in cerebellar lobule IV/V.
Increased Purkinje cell (PC) mislocalization and decreased parvalbumin in molecular layer interneurons (MLIs) were observed in lobule VI.
16p11.2^dp/+ mice exhibited deficits in conditioned response percentage and onset latency during delay eyeblink conditioning.

Conclusions:

Lobule VI-specific alterations in PC localization and MLI parvalbumin expression may underlie impaired associative learning in 16p11.2^dp/+ mice.
These findings suggest a potential role for cerebellar dysfunction in the pathogenesis of neuropsychiatric disorders associated with 16p11.2 microduplication.