Stodieck Sophia Katharina, Greifzu Franziska, Goetze Bianka, Schmidt Karl-Friedrich, Löwel Siegrid
Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences, Justus-von-Liebig-Weg 11, D-37077 Göttingen, Germany; Bernstein Fokus Neurotechnologie (BFNT) and Johann-Friedrich-Blumenbach Institut für Zoologie und Anthropologie, Universität Göttingen, Von-Siebold-Str. 6, D-37075 Göttingen, Germany.
Bernstein Fokus Neurotechnologie (BFNT) and Johann-Friedrich-Blumenbach Institut für Zoologie und Anthropologie, Universität Göttingen, Von-Siebold-Str. 6, D-37075 Göttingen, Germany.
Exp Gerontol. 2014 Dec;60:1-11. doi: 10.1016/j.exger.2014.09.007. Epub 2014 Sep 16.
In the primary visual cortex (V1), monocular deprivation (MD) induces a shift in the ocular dominance (OD) of binocular neurons towards the open eye (Wiesel and Hubel, 1963; Gordon and Stryker, 1996). In V1 of C57Bl/6J mice, this OD-plasticity is maximal in juveniles, declines in adults and is absent beyond postnatal day (PD) 110 (Lehmann and Löwel, 2008) if mice are raised in standard cages. Since it was recently shown that brief dark exposure (DE) restored OD-plasticity in young adult rats (PD70-100) (He et al., 2006), we wondered whether DE would restore OD-plasticity also in adult and old mice and after a cortical stroke. To this end, we raised mice in standard cages until adulthood and transferred them to a darkroom for 10-14 days. Using intrinsic signal optical imaging we demonstrate that short-term DE can restore OD-plasticity after MD in both adult (PD138) and old mice (PD535), and that OD-shifts were mediated by an increase of open eye responses in V1. Interestingly, restored OD-plasticity after DE was accompanied by a reduction of both parvalbumin expressing cells and perineuronal nets and was prevented by increasing intracortical inhibition with diazepam. DE also maintained OD-plasticity in adult mice (PD150) after a stroke in the primary somatosensory cortex. In contrast, short-term DE did not affect basic visual parameters as measured by optomotry. In conclusion, short-term DE was able to restore OD-plasticity in both adult and aging mice and even preserved plasticity after a cortical stroke, most likely mediated by reducing intracortical inhibition.
在初级视觉皮层（V1）中，单眼剥夺（MD）会导致双眼神经元的眼优势（OD）向睁开的眼睛偏移（维泽尔和休伯尔，1963年；戈登和斯特里克，1996年）。在C57Bl/6J小鼠的V1中，如果小鼠饲养在标准笼中，这种OD可塑性在幼年时最大，成年后下降，在出生后第110天（PD）之后消失（莱曼和勒韦尔，2008年）。由于最近有研究表明，短暂黑暗暴露（DE）可恢复年轻成年大鼠（PD70 - 100）的OD可塑性（何等人，2006年），我们想知道DE是否也能恢复成年和老年小鼠以及皮质中风后的OD可塑性。为此，我们将小鼠饲养在标准笼中直至成年，然后将它们转移到暗室中10 - 14天。使用内在信号光学成像，我们证明短期DE可以恢复成年（PD138）和老年小鼠（PD535）在MD后的OD可塑性，并且OD偏移是由V1中睁开眼睛反应的增加介导的。有趣的是，DE后恢复的OD可塑性伴随着表达小白蛋白的细胞和神经元周围网络的减少，并且通过地西泮增加皮质内抑制作用可阻止这种现象。在初级体感皮层中风后，DE也能维持成年小鼠（PD150）的OD可塑性。相比之下，短期DE并不影响通过视动性测量的基本视觉参数。总之，短期DE能够恢复成年和衰老小鼠的OD可塑性，甚至在皮质中风后仍能保持可塑性，最有可能是通过减少皮质内抑制作用介导的。
