title: Acute Cortical Transhemispheric Diaschisis after Unilateral Traumatic Brain Injury.
abstract: Focal neocortical brain injuries lead to functional alterations, which can spread beyond lesion-neighboring brain areas. The undamaged hemisphere and its associated disturbances after a unilateral lesion, so-called transhemispheric diaschisis, have been progressively disclosed over the last decades; they are strongly involved in the pathophysiology and, potentially, recovery of brain injuries. Understanding the temporal dynamics of these transhemispheric functional changes is crucial to decipher the role of the undamaged cortex in the processes of functional reorganization at different stages post-lesion. In this regard, little is known about the acute-subacute processes after 24-48 h in the brain hemisphere contralateral to injury. In the present study, we performed a controlled cortical impact to produce a unilateral traumatic brain injury (TBI) in the motor and somatosensory cortex of mice. In vitro extracellular multi-unit recordings from large neuronal populations, together with single-cell patch-clamp recordings in the cortical network contralateral to the lesion, revealed a strong, but transient, neuronal hyperactivity as early as 24-48 h post-TBI. This abnormal excitable state in the intact hemisphere was not accompanied by alterations in neuronal intrinsic properties, but it was associated with an impairment of the phasic gamma aminobutyric acid (GABA)ergic transmission and an increased expression of GABAAreceptor subunits related to tonic inhibition exclusively in the contralateral hemisphere. These data unravel a series of early transhemispheric functional alterations after diffuse unilateral cortical injury, which may compensate and stabilize the disrupted brain functions. Therefore, our findings support the hypothesis that the undamaged hemisphere could play a significant role in early functional reorganization processes after a TBI.
authors.affiliation: 1 Institute for Physiology, UMC of the Johannes Gutenberg University Mainz , Mainz, Germany .
authors.forename: Florie
authors.initials: F
authors.lastname: Le Prieult
authors.affiliation: 2 Department of Anesthesiology, University Medical Center of Johannes Gutenberg University , Mainz, Germany .
authors.forename: Serge C
authors.initials: SC
authors.lastname: Thal
authors.affiliation: 2 Department of Anesthesiology, University Medical Center of Johannes Gutenberg University , Mainz, Germany .
authors.forename: Kristin
authors.initials: K
authors.lastname: Engelhard
authors.affiliation: 1 Institute for Physiology, UMC of the Johannes Gutenberg University Mainz , Mainz, Germany .|3 Current affiliation for B.I.: Neurowissenschaftliches Forschungszentrum, University Medical Center of Charité Berlin, Campus Charité Mitte, Berlin, Germany.
authors.forename: Barbara
authors.initials: B
authors.lastname: Imbrosci
authors.affiliation: 1 Institute for Physiology, UMC of the Johannes Gutenberg University Mainz , Mainz, Germany .
authors.forename: Thomas
authors.initials: T
authors.lastname: Mittmann
mesh_terms: D000818:Animals; D000070642:Brain Injuries, Traumatic / Q000473:pathology* / Q000503:physiopathology*; D004195:Disease Models, Animal; D004569:Electroencephalography; D008810:Mice, Inbred C57BL; D009044:Motor Cortex / Q000293:injuries* / Q000503:physiopathology*; D009473:Neuronal Plasticity; D018408:Patch-Clamp Techniques; D013003:Somatosensory Cortex / Q000293:injuries* / Q000503:physiopathology*
keywords: electrophysiology; neuroplasticity; traumatic brain injury