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Crybb2 Mutations Consistently Affect Schizophrenia Endophenotypes in Mice.

Tamara Heermann1,2, Lillian Garrett1,3, Wolfgang Wurst1,4,5,6

  • 1Institute of Developmental Genetics, Helmholtz Zentrum München, German Research Centre for Environmental Health, 85764, Neuherberg, Germany.

Molecular Neurobiology
|October 7, 2018
PubMed
Summary
This summary is machine-generated.

Mutations in the beta B2-crystallin (CRYBB2) gene, linked to cataracts, also affect brain function. Altered CRYBB2 impacts sensorimotor gating and parvalbumin-positive neuron counts, suggesting a role in schizophrenia development.

Keywords:
Crybb2ParvalbuminPrepulse inhibition (PPI)SchizophreniaThalamic reticular nucleus (TRN)

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Area of Science:

  • Neuroscience
  • Genetics
  • Ophthalmology

Background:

  • Beta B2-crystallin (CRYBB2) is an ocular protein associated with cataracts.
  • CRYBB2 is also found in the adult mouse brain and linked to neuropsychiatric disorders like schizophrenia.
  • The precise role of CRYBB2 in brain function and its contribution to disease phenotypes remain unclear.

Purpose of the Study:

  • To investigate the behavioral and neurohistological effects of Crybb2 gene mutations.
  • To explore the association between Crybb2 mutations and schizophrenia-related endophenotypes.

Main Methods:

  • Generated and analyzed three lines of mice with distinct Crybb2 gene mutations (Crybb2O377, Crybb2Philly, Crybb2Aey2).
  • Conducted behavioral tests including open field, acoustic startle reflex (prepulse inhibition - PPI), social discrimination, and Y-maze.
  • Quantified parvalbumin-positive (PV+) GABAergic interneurons in specific brain regions expressing CRYBB2.

Main Results:

  • All three mutant lines showed consistent alterations in PPI, a measure of sensorimotor gating.
  • These PPI alterations correlated with changes in the number of PV+ cells in the thalamic reticular nucleus (TRN).
  • Allele-specific differences in behavior and brain region involvement were observed across mutant lines.

Conclusions:

  • Altered numbers of PV+ cells in the TRN appear to modulate PPI.
  • The findings implicate mutations in the Crybb2 gene in the development of schizophrenia, given that altered PPI and PV+ cell counts are known endophenotypes of the disorder.