title: Short- and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia.
abstract: Evoked potentials recorded from the somatosensory cortex have been shown to be an electrophysiological marker of brain injury in global hypoxic ischemia (HI). The evoked responses in somatosensory neurons carry information pertaining to signal from the ascending pathway in both the subcortical and cortical areas. In this study, origins of the subcortical and cortical signals are explored by decomposing the evoked neuronal activities into short- and long-latency responses (SLR and LLR), respectively. We evaluated the effect of therapeutic hypothermia on SLR and LLR during early recovery from cardiac arrest (CA)-induced HI in a rodent model. Twelve rats were subjected to CA, after which half of them were treated with hypothermia (32-34°C) and the rest were kept at normal temperature (36-37°C). Evoked neuronal activities from the primary somatosensory cortex, including multiunit activity (MUA) and local field potential (LFP), were continuously recorded during injury and early recovery. Results showed that upon initiation of injury, LLR disappeared first, followed by the disappearance of SLR, and after a period of isoelectric silence SLR reappeared prior to LLR. This suggests that cortical activity, which primarily underlies the LLR, may be more vulnerable to ischemic injury than SLR, which relates to subcortical activity. Hypothermia potentiated the SLR but suppressed the LLR by delaying its recovery after CA (hypothermia: 38.83 ± 5.86 min, normothermia: 23.33 ± 1.15 min; P < 0.05) and attenuating its amplitude, suggesting that hypothermia may selectively downregulate cortical activity as an approach to preserve the cerebral cortex. In summary, our study reveals the vulnerability of the somatosensory neural structures to global HI and the differential effects of hypothermia on these structures.
authors.affiliation: Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
authors.forename: Dan
authors.initials: D
authors.lastname: Wu
authors.forename: Wei
authors.initials: W
authors.lastname: Xiong
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Jia
authors.forename: Romergryko G
authors.initials: RG
authors.lastname: Geocadin
authors.forename: Nitish V
authors.initials: NV
authors.lastname: Thakor
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001930:Brain Injuries / Q000209:etiology / Q000473:pathology*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D007839:Functional Laterality; D006614:Hindlimb / Q000294:innervation; D007036:Hypothermia, Induced / Q000379:methods*; D020925:Hypoxia-Ischemia, Brain / Q000150:complications / Q000628:therapy*; D008297:Male; D009474:Neurons / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000502:physiology*; D013003:Somatosensory Cortex / Q000473:pathology / Q000503:physiopathology*; D018709:Statistics, Nonparametric; D013997:Time Factors