caa a22 4500 606202242 CHVBK 20210128100952.0 cr unu---uuuuu 210128e20150501xx s 000 0 eng 10.1007/s00429-014-0750-8 doi (NATIONALLICENCE)springer-10.1007/s00429-014-0750-8 Neuronal mechanisms underlying transhemispheric diaschisis following focal cortical injuries [Elektronische Daten] [Barbara Imbrosci, Ellen Ytebrouck, Lutgarde Arckens, Thomas Mittmann] Unilateral cortical lesions cause disturbances often spreading into the hemisphere contralateral to the injury. The functional alteration affecting the contralesional cortex is called transhemispheric diaschisis and is believed to contribute to neurological deficits and to processes of functional reorganization post-lesion. Despite the profound implications for recovery, little is known about the cellular mechanisms that underlie this phenomenon. In the present study, transhemispheric diaschisis was investigated with an in vivo-ex vivo model of unilateral lesions, induced by an infrared laser in rat visual cortex. Visually evoked cortical activity was evaluated by the expression level of the cellular activity marker zif268, which showed an elevation in the cortex contralateral to the lesion. In vitro patch-clamp recordings from layer 2/3 pyramidal neurons revealed a shift in the excitatory-inhibitory balance in favor of excitability, particularly expressed in the undamaged hemisphere. Layer 5 principal neurons displayed an increased spontaneous firing rate contralateral to the lesion, while cells of the injured cortex displayed a reduced firing upon somatic current injection. These data suggest that a cortical lesion triggers an enhanced neuronal activity in the hemisphere contralateral to the damage. Our findings constitute an important step toward the understanding of transhemispheric diaschisis on the cellular level. Springer-Verlag Berlin Heidelberg, 2014 Cortical injuries nationallicence Transhemispheric diaschisis nationallicence zif268 nationallicence Patch-clamp recordings nationallicence Imbrosci Barbara Institute for Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Duesbergweg 6, 55128, Mainz, Germany aut Ytebrouck Ellen Laboratory of Neuroplasticity and Neuroproteomics, KU Leuven, Naamsestraat 59, 3000, Leuven, Belgium aut Arckens Lutgarde Laboratory of Neuroplasticity and Neuroproteomics, KU Leuven, Naamsestraat 59, 3000, Leuven, Belgium aut Mittmann Thomas Institute for Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Duesbergweg 6, 55128, Mainz, Germany aut Brain Structure and Function Springer Berlin Heidelberg 220/3(2015-05-01), 1649-1664 1863-2653 220:3<1649 2015 220 429 https://doi.org/10.1007/s00429-014-0750-8 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00429-014-0750-8 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Imbrosci Barbara Institute for Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Duesbergweg 6, 55128, Mainz, Germany aut NATIONALLICENCE 700 1- Ytebrouck Ellen Laboratory of Neuroplasticity and Neuroproteomics, KU Leuven, Naamsestraat 59, 3000, Leuven, Belgium aut NATIONALLICENCE 700 1- Arckens Lutgarde Laboratory of Neuroplasticity and Neuroproteomics, KU Leuven, Naamsestraat 59, 3000, Leuven, Belgium aut NATIONALLICENCE 700 1- Mittmann Thomas Institute for Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Duesbergweg 6, 55128, Mainz, Germany aut NATIONALLICENCE 773 0- Brain Structure and Function Springer Berlin Heidelberg 220/3(2015-05-01), 1649-1664 1863-2653 220:3<1649 2015 220 429