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Transcranial Direct Current Stimulation Attenuates Ischemic Stroke-Induced Autonomic and Behavioral Dysfunction via a

Yun Hsu1, Chou-Ching Lin2,3, Chih-Hsu Huang2,3

  • 1Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

Journal of Neurochemistry
|May 29, 2026
PubMed
Summary

Ischemic stroke disrupts brainstem autonomic regulation, leading to high blood pressure. Non-invasive brain stimulation (tDCS) can restore molecular balance in the rostral ventrolateral medulla (RVLM), mitigating stroke effects.

Keywords:
autophagyiron homeostasisischemic strokerenin–angiotensin systemrostral ventrolateral medullatranscranial direct current stimulation

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Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Ischemic stroke often causes sympathetic overactivity and blood pressure dysregulation.
  • This is linked to impaired autonomic control in the brainstem's rostral ventrolateral medulla (RVLM).
  • The precise molecular mechanisms driving this dysfunction are not fully understood.

Purpose of the Study:

  • To investigate the interplay of the renin-angiotensin system (RAS), autophagy, and iron metabolism in the RVLM following ischemic stroke.
  • To explore the effects of transcranial direct current stimulation (tDCS) on these molecular pathways in the context of stroke.

Main Methods:

  • Utilized a transient middle cerebral artery occlusion (MCAO) rat model to simulate ischemic stroke.
  • Analyzed molecular changes in the RVLM, including RAS signaling, autophagic flux, and iron metabolism.
  • Assessed the impact of transcranial direct current stimulation (tDCS) on these parameters post-stroke.

Main Results:

  • Stroke induced RAS imbalance, disrupted autophagic flux, and altered iron storage proteins in the RVLM.
  • These molecular changes correlated with elevated blood pressure and sympathetic dysregulation.
  • tDCS treatment normalized RAS signaling, restored autophagic activity (including ferritin degradation), and reduced iron-associated oxidative stress.

Conclusions:

  • Stroke triggers a molecular cascade in the RVLM involving RAS, autophagy, and iron metabolism, contributing to sympathetic overactivity.
  • tDCS shows potential as a non-invasive therapy to restore neurochemical homeostasis in the RVLM after stroke.
  • These findings offer insights into stroke-related autonomic dysfunction and potential therapeutic interventions.