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RESEARCH PRODUCT
Acute Cortical Transhemispheric Diaschisis after Unilateral Traumatic Brain Injury
Serge C. ThalFlorie Le PrieultThomas MittmannKristin EngelhardBarbara ImbrosciBarbara Imbroscisubject
0301 basic medicinePatch-Clamp TechniquesTraumatic brain injurySomatosensory system03 medical and health sciences0302 clinical medicineCortex (anatomy)Unilateral lesionBrain Injuries TraumaticNeuroplasticitymedicineAnimalsDiaschisisNeuronal PlasticityMotor CortexElectroencephalographySomatosensory Cortexmedicine.diseaseMice Inbred C57BLDisease Models AnimalElectrophysiology030104 developmental biologymedicine.anatomical_structureBrain HemisphereNeurology (clinical)PsychologyNeuroscience030217 neurology & neurosurgerydescription
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 GABA
year | journal | country | edition | language |
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2017-03-01 | Journal of Neurotrauma |