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Vagus Nerve Stimulation as a Tool to Induce Plasticity in Pathways Relevant for Extinction Learning
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A brainstem circuit for nausea suppression.

Chuchu Zhang1, Lindsay K Vincelette1, Frank Reimann2

  • 1Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

Cell Reports
|June 15, 2022
PubMed
Summary
This summary is machine-generated.

Researchers discovered inhibitory neurons in the brainstem that counteract nausea. The gut hormone glucose insulinotropic peptide (GIP) activates these neurons, blocking nausea responses to poisons and offering a new target for nausea intervention.

Keywords:
CP: NeuroscienceGDF15GFRALGIPRchannelrhodopsin-assisted circuit mappingcircumventricular organconditioned flavor avoidancegrowth/differentiation factor 15sickness behavior

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Area of Science:

  • Neuroscience
  • Gastroenterology
  • Pharmacology

Background:

  • Nausea is a significant clinical challenge, often triggered by toxins acting on the area postrema.
  • The area postrema, a sensory organ, detects bloodborne factors and plays a key role in nausea induction.

Purpose of the Study:

  • To identify neural circuits in the area postrema that regulate nausea responses.
  • To investigate the role of the gut hormone glucose insulinotropic peptide (GIP) in modulating nausea.

Main Methods:

  • Utilized genetic approaches and an area postrema cell atlas.
  • Performed targeted ablation of specific neurons in the area postrema.
  • Measured behavioral responses to poisons in mice.

Main Results:

  • Identified inhibitory neurons within the area postrema that counteract nausea.
  • Demonstrated that glucose insulinotropic peptide (GIP) activates these inhibitory neurons via GABA receptors.
  • Showed that GIP administration blocks poison-induced nausea behaviors, an effect abolished by neuron ablation.

Conclusions:

  • Area postrema inhibitory neurons are crucial in regulating nausea responses to toxins.
  • GIP-activated inhibitory pathways in the area postrema offer a potential therapeutic strategy for nausea intervention.