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Awakening Recovery: Enhancing Orexinergic Tone After Acute CNS Damage.

Paloma Otero-López1,2, Xavier Madrid-González1,2, Víctor Fernández-Dueñas1,2

  • 1Pharmacology Unit, Department of Pathology and Experimental Therapeutics, School of Medicine and Health Sciences, Institute of Neurosciences, Universitat de Barcelona, 08907 Barcelona, Spain.

Pharmaceuticals (Basel, Switzerland)
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PubMed
Summary
This summary is machine-generated.

Orexin (hypocretin) signaling is suppressed after acute central nervous system (CNS) injuries but enhancing it may stabilize arousal and support recovery. Targeting orexin pathways offers a phase-sensitive approach for CNS injury treatment.

Keywords:
acute CNS injuryarousalneuroprotectionneurorehabilitationorexin receptor agonistsorexin/hypocretinspinal cord injurystroketraumatic brain injury

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Area of Science:

  • Neuroscience
  • Neuromodulation
  • Neuroimmunology

Background:

  • Acute central nervous system (CNS) injuries disrupt arousal, autonomic stability, and neuroimmune balance.
  • The orexin (hypocretin) network is crucial for wakefulness, autonomic control, and motivated behaviors.
  • Orexin signaling is suppressed following various CNS injuries, including ischemic, hemorrhagic, and traumatic events.

Purpose of the Study:

  • To review the role of orexin signaling in acute CNS injuries.
  • To synthesize evidence on the effects of enhancing orexinergic tone on arousal, inflammation, and behavior.
  • To examine strategies for modulating orexin pathways for therapeutic benefit.

Main Methods:

  • Literature review synthesizing experimental evidence across multiple CNS injury models (ischemia, hemorrhage, trauma, systemic inflammation).
  • Analysis of pharmacological, peptide-based, neuromodulatory, and physiological strategies to enhance orexinergic tone.
  • Integration of findings within a timing-aware framework across different injury etiologies.

Main Results:

  • Orexin signaling is sharply suppressed early post-injury, gradually recovering with stabilization of arousal and homeostatic functions.
  • Controlled enhancement of orexinergic tone can improve arousal, modulate inflammation, and support behavioral engagement, contingent on timing and context.
  • Selective OX2 agonists and methods to boost endogenous orexin activity are under development.

Conclusions:

  • Orexin pathways are uniquely positioned to integrate arousal, autonomic control, and motivated behavior following CNS injury.
  • Targeting orexin offers a phase-sensitive therapeutic strategy to stabilize arousal and promote recovery across diverse CNS injuries.
  • Orexin modulation may complement existing therapies by linking early stabilization with long-term functional recovery.