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Brain Circuitry for Arousal from Apnea.

Clifford B Saper1, Satvinder Kaur1

  • 1Department of Neurology, Division of Sleep Medicine, and Program in Neuroscience, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.

Cold Spring Harbor Symposia on Quantitative Biology
|April 25, 2019
PubMed
Summary

This study reveals that specific neurons in the brainstem

Area of Science:

  • Neuroscience
  • Respiratory Physiology
  • Sleep Medicine

Background:

  • The brainstem plays a crucial role in regulating vital functions, including arousal and cardiorespiratory control.
  • Elevated carbon dioxide (CO2) or low oxygen (O2) levels trigger arousal responses, essential for survival but implicated in conditions like sleep apnea.
  • The parabrachial nucleus (PB) is a key integration center for chemosensory information related to CO2 and O2.

Purpose of the Study:

  • To elucidate the specific neural circuits mediating arousal from hypercapnia (high CO2) and hypoxia (low O2).
  • To identify the role of parabrachial nucleus (PB) neurons expressing calcitonin gene-related peptide (CGRP) in arousal responses.
  • To investigate the downstream targets of PB neurons involved in awakening.

Main Methods:

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  • Genetic manipulation to delete vesicular glutamate transporter 2 in PB neurons.
  • Utilizing CGRP-Cre-ER mice to target specific neuronal populations.
  • Employing optogenetic techniques (photoinhibition) to selectively inhibit PB CGRP neurons and their projections.
  • Measuring cFos expression as a marker of neuronal activity during high CO2 exposure.

Main Results:

  • Deletion of vesicular glutamate transporter 2 in PB neurons abolished arousal to high CO2 and low O2.
  • PB neurons expressing CGRP (PB CGRP neurons) were activated during high CO2 exposure.
  • Optogenetic inhibition of PB CGRP neurons or their projections to the basal forebrain, amygdala, and lateral hypothalamus prevented awakening to high CO2.
  • PB CGRP neurons are critical for mediating arousal responses to apnea-like conditions.

Conclusions:

  • PB CGRP neurons are essential components of the neural circuitry that triggers awakening in response to respiratory challenges.
  • These findings identify a specific neuronal pathway involved in the vital response to hypoxia and hypercapnia.
  • Targeting the PB CGRP pathway may offer novel therapeutic strategies for sleep-related breathing disorders.