Spreading depressions and periinfarct spreading depolarizations in the context of cortical plasticity

Abstract

AbstractStudies of cortical function-recovery require a comparison between normal and post-stroke conditions that lead to changes in cortical metaplasticity. Focal cortical stroke impairs experience-dependent plasticity (ExDP) in the neighboring somatosensory cortex and usually evokes periinfarct depolarizations (PiDs) – a spreading depression-like waves. Experimentally induced spreading depressions (SDs) affect gene expression and some of these changes persist for at least 30 days. However, such changes are not stroke-specific: migraine patients had prolonged protein changes after a single SD episode during migraine aura. This study investigates whether non-stroke depolarizations impair cortical ExDP similarly to the stroke.ExDP was induced in rates with SDs or PiDs by a month of contralateral partial whiskers deprivation. Cortical activity was mapped by [14C]-2-deoxy-D-glucose (2DG) incorporation during stimulation of spared and contralateral homotopic whiskers. We found that whiskers deprivation after SDs resulted in normal cortical representation enlargement suggesting that SDs and PiDs depolarization have no influence on ExDP cortical map reorganization. PiDs and the MMP-9, −3, −2 or COX-2 proteins which are assumed to influence metaplasticity in rats after stroke were compared between the SDs induced by high osmolarity KCl solution and the PiDs following cortical photothrombotic stroke (PtS). We found that none of these factors directly caused cortical post-stroke metaplasticity changes. The only significant difference between stoke and induced SD was a greater imbalance in interhemispheric activity equilibrium after stroke. The interhemispheric interactions modified by stroke may therefore be a promising target for future studies of post-stroke ExDP and for convalescence studies.HighlightsPost-stroke metaplasticity changes in an injured hemisphere are not a consequence of spreading depolarizationsNone of the monitored proteins (MMP-2, -3, -9; COX-2) cause modifications in poststroke cortical plasticitySpreading depressions have a prolonged, global influence on the functioning of both hemispheres and of the thalamusImpaired interhemispheric interactions may underlie the post-stroke metaplasticity changes in the injured hemisphere