title: High-frequency cortical stimulation augments recovery of thalamocortical oscillations from hypoxia in rat brain slices.
abstract: OBJECTIVE
  Cerebrovascular hypoxia results in severe impairment and electrical dysfunction of cortical and thalamic neuronal networks. Typically cellular electrical activity returns if reoxygenation is established within 5-8 min. Electrical stimulation has been shown to reduce cellular apoptosis following cerebral hypoxia in animal models and clinical case reports. In this study, we wanted to analyze the electrophysiological repercussions of electrical stimulation on recovery of spontaneous thalamocortical oscillations (TCOs) following hypoxia in a thalamocortical slice preparation.
  
  
  METHODS
  A hypoxia model of rat thalamocortical brain slices was used in which spontaneous TCO and cortical oscillation (CO) activity could be tracked with extracellular and intracellular recording techniques. Spontaneous TCO and CO activity was recorded prior to, during, and after hypoxia was induced in 15 brain slices. Bipolar, high-frequency stimulation (100 µsec, 150 Hz, 3 V) of somatosensory cortex was applied immediately after reoxygenation of slices was started and its effect on return of TCO activity compared with non-stimulated slices.
  
  
  RESULTS
  Depolarization and suppression of extracellular TCOs and COs were demonstrated following the induction of hypoxia. TCO activity was lost after an average of 2.7 ± 0.5 min of hypoxia, whereas COs activity remained for an additional 3.2 ± 0.3 min in the presence of hypoxia. After loss of both TCOs and COs, oxygenated perfusate was restarted and TCOs spontaneously recovered in 6.8 ± 0.42 min. When 10 sec of high-frequency cortical stimulation was applied at the beginning of oxygenated perfusion, TCOs were observed to recover within 2.8 ± 0.76 min. If oxygenated perfusate was not restarted within 2 min following loss of either TCOs or COs, no recovery was seen.
  
  
  CONCLUSIONS
  High-frequency cortical stimulation accelerated the recovery of thalamocortical network activity following hypoxia and reperfusion. Insight into the underlying mechanisms of this effect may enhance therapeutic interventions related to hypoxia following ischemic stroke.
authors: Department of Neurosurgery, Vanderbilt University, Nashville, TN 37232, USA. chris.kao@vanderbilt.edu
authors: Chris
authors: C
authors: Kao
authors: Jonathan A
authors: JA
authors: Forbes
authors: Aaron
authors: A
authors: Stayman
authors: David A
authors: DA
authors: Sun
authors: Romain
authors: R
authors: Carron
authors: Alim Louis
authors: AL
authors: Benabid
authors: Peter
authors: P
authors: Konrad
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology* / Q000503:physiopathology*; D004558:Electric Stimulation / Q000379:methods*; D005260:Female; D006801:Humans; D002534:Hypoxia, Brain / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009415:Nerve Net / Q000502:physiology; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D013788:Thalamus / Q000502:physiology* / Q000503:physiopathology*