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Brn3b regulates the formation of fear-related midbrain circuits and defensive responses to visual threat

Hyoseo Lee1, Hannah Weinberg-Wolf1, Hae-Lim Lee2

  • 1Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut, United States of America.

Plos Biology
|November 20, 2023
PubMed

Insights

The transcription factor Brn3b is crucial for developing midbrain circuits that control defensive behaviors. Its absence impairs fear responses, but this can be restored by increasing tachykinin 2 (Tac2) levels.

Area of Science:

  • Neuroscience
  • Genetics
  • Behavioral Biology

Background:

  • Defensive responses to visual threats are vital survival instincts across species.
  • Midbrain neural circuits mediate visually triggered defensive behaviors, but their molecular regulation is unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms controlling the development and function of midbrain fear circuits.
  • To identify genetic components essential for visually triggered defensive responses.

Main Methods:

  • Midbrain-specific deletion of the transcription factor Brn3b in mice.
  • Analysis of neuronal projections to the lateral posterior nucleus of the thalamus.
  • Assessment of defensive freezing behavior in response to visual threat.
  • Tachykinin 2 (Tac2) expression analysis and manipulation.

Main Results:

  • Brn3b deletion resulted in the loss of neurons projecting to the thalamus.
  • Tac2 expression was downregulated following Brn3b deletion.
  • Brn3b mutant mice showed impaired freezing responses to visual threat.
  • Overexpression of Tac2 ameliorated the behavioral deficits in Brn3b mutant mice.

Conclusions:

  • Brn3b is critical for the development and function of midbrain fear circuits.
  • Tac2 acts downstream of Brn3b in regulating defensive responses to threat.
  • These findings identify key genetic regulators of fear-related visual circuits.

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