Abstract
Neuronal plasticity is essential to enable rehabilitation when the brain suffers from injury, such as following a stroke. One of the most established models to study cortical plasticity is ocular dominance (OD) plasticity in the primary visual cortex (V1) of the mammalian brain induced by monocular deprivation (MD). We have previously shown that OD-plasticity in adult mouse V1 is absent after a photothrombotic (PT) stroke lesion in the adjacent primary somatosensory cortex (S1). Exposing lesioned mice to conditions which reduce the inhibitory tone in V1, such as raising animals in an enriched environment or short-term dark exposure, preserved OD-plasticity after an S1-lesion. Here we tested whether modification of excitatory circuits can also be beneficial for preserving V1-plasticity after stroke. Mice lacking postsynaptic density protein-95 (PSD-95), a signaling scaffold present at mature excitatory synapses, have lifelong juvenile-like OD-plasticity caused by an increased number of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) -silent synapses in V1 but unaltered inhibitory tone. In fact, using intrinsic signal optical imaging, we show here that OD-plasticity was preserved in V1 of adult PSD-95 KO mice after an S1-lesion but not in PSD-95 wildtype (WT)-mice. In addition, experience-enabled enhancement of the optomotor reflex of the open eye after MD was compromised in both lesioned PSD-95 KO and PSD-95 WT mice. Basic V1-activation and retinotopic map quality were, however, not different between lesioned PSD-95 KO mice and their WT littermates. The preserved OD-plasticity in the PSD-95 KO mice indicates that V1-plasticity after a distant stroke can be promoted by either changes in excitatory circuitry or by lowering the inhibitory tone in V1 as previously shown. Furthermore, the present data indicate that an increased number of AMPA-silent synapses preserves OD-plasticity not only in the healthy brain, but also in another experimental paradigm of cortical plasticity, namely the long-range influence on V1-plasticity after an S1-lesion.
Highlights
If the brain is injured, for example due to a stroke lesion, neuronal plasticity is crucial for recovery and to promote rehabilitation
In adult PSD-95 KO mice, ocular dominance plasticity in V1 was preserved after a stroke lesion in S1 In S1-lesioned PSD-95 WT mice, OD-plasticity in V1 was absent, as previously described for WT mice [6]
Our results demonstrate that OD-plasticity in V1 after a cortical stroke lesion in the adjacent S1-area is preserved in PSD-95 KO mice but not in PSD-95 WT mice
Summary
If the brain is injured, for example due to a stroke lesion, neuronal plasticity is crucial for recovery and to promote rehabilitation. We observed that a small photothrombotic (PT) stroke lesion in S1, directly adjacent to V1, or even in M2, nearly 4 mm anterior to the anterior border of V1, abolished OD-plasticity in V1 and impaired experience-enabled improvements of the optomotor reflex of the open eye after MD in adult mice [6, 7]. We tested whether knockout (KO) mice for PSD-95 display a preserved OD-plasticity in V1 after a small lesion in S1, adjacent to V1 To this end, we induced a photothrombotic stroke lesion in S1, about 1 mm anterior to the anterior border of V1 and visualized ODplasticity using in vivo optical imaging of intrinsic signals. Experience-enabled changes of the optomotor reflex were compromised in both S1-lesioned PSD-95 KO and PSD-95 WT mice after MD
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