TY - JOUR
T1 - Brainstem and cortical spreading depolarization in a closed head injury rat model
AU - Aboghazleh, Refat
AU - Parker, Ellen
AU - Yang, Lynn T.
AU - Kaufer, Daniela
AU - Dreier, Jens P.
AU - Friedman, Alon
AU - van Hameren, Gerben
N1 - Funding Information:
Funding: This work was supported by the Canadian Institute for Health Research PJT 148896 and by the U.S. Army Medical Research Acquisition Activity Office, 820 Chandler Street, Fort Detrick MD 21702-5014, as the awarding and administering acquisition office of the Assistant Secretary of Defense for Health Affairs, through the Epilepsy Research Program, under Award No. W81XWH-17-1-0684. Opinions, interpretations, conclusions, and recommendations are those of the author, and are not necessarily endorsed by the Department of Defense. In addition, the study was supported by the Deutsche Forschungsgemeinschaft (DFG DR 323/5-1, DFG DR 323/10-1), the European Commission (FP7 no 602150 CENTER-TBI), BMBF Bundesministerium für Bildung und Forschung (Era-Net Neuron EBio2, with funds from BMBF 01EW2004 and CIHR NDD-168164), and Mitacs Accelerate (IT13603). In conducting research using animals, the investigators adhered to the laws of the United States and the regulations of the Department of Agriculture.
Funding Information:
This work was supported by the Canadian Institute for Health Research PJT 148896 and by the U.S. Army Medical Research Acquisition Activity Office, 820 Chandler Street, Fort Detrick MD 21702-5014, as the awarding and administering acquisition office of the Assistant Secretary of Defense for Health Affairs, through the Epilepsy Research Program, under Award No. W81XWH-17-1-0684. Opinions, interpretations, conclusions, and recommendations are those of the author, and are not necessarily endorsed by the Department of Defense. In addition, the study was supported by the Deutsche Forschungsgemeinschaft (DFG DR 323/5-1, DFG DR 323/10-1), the European Commission (FP7 no 602150 CENTER-TBI), BMBF Bundesministerium f?r Bildung und Forschung (Era-Net Neuron EBio2, with funds from BMBF 01EW2004 and CIHR NDD-168164), and Mitacs Accelerate (IT13603). In conducting research using animals, the investigators adhered to the laws of the United States and the regulations of the Department of Agriculture.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/11/1
Y1 - 2021/11/1
N2 - Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been fully elucidated. To investigate the electrophysiological events that immediately follow traumatic brain injury, a weight-drop model of traumatic brain injury was used in rats pre-implanted with epidural and intracerebral electrodes. Electrophysiological (near-direct current) recordings and simultaneous alternating current recordings of brain activity were started within seconds following impact. Cortical spreading depolarization (SD) and SD-induced spreading depression occurred in approximately 50% of mild and severe impacts. SD was recorded within three minutes after injury in either one or both brain hemispheres. Electrographic seizures were rare. While both TBI-and electrically induced SDs resulted in elevated oxidative stress, TBI-exposed brains showed a reduced antioxidant defense. In severe TBI, brainstem SD could be recorded in addition to cortical SD, but this did not lead to the death of the animals. Severe impact, however, led to immediate death in 24% of animals, and was electrocorticographically characterized by non-spreading depression (NSD) of activity followed by terminal SD in both cortex and brainstem.
AB - Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been fully elucidated. To investigate the electrophysiological events that immediately follow traumatic brain injury, a weight-drop model of traumatic brain injury was used in rats pre-implanted with epidural and intracerebral electrodes. Electrophysiological (near-direct current) recordings and simultaneous alternating current recordings of brain activity were started within seconds following impact. Cortical spreading depolarization (SD) and SD-induced spreading depression occurred in approximately 50% of mild and severe impacts. SD was recorded within three minutes after injury in either one or both brain hemispheres. Electrographic seizures were rare. While both TBI-and electrically induced SDs resulted in elevated oxidative stress, TBI-exposed brains showed a reduced antioxidant defense. In severe TBI, brainstem SD could be recorded in addition to cortical SD, but this did not lead to the death of the animals. Severe impact, however, led to immediate death in 24% of animals, and was electrocorticographically characterized by non-spreading depression (NSD) of activity followed by terminal SD in both cortex and brainstem.
KW - Brainstem
KW - Cortical spreading depolarization
KW - Electrocorticography
KW - Oxidative stress
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=85117945496&partnerID=8YFLogxK
U2 - 10.3390/ijms222111642
DO - 10.3390/ijms222111642
M3 - Article
C2 - 34769073
AN - SCOPUS:85117945496
SN - 1661-6596
VL - 22
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 21
M1 - 11642
ER -