Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

School of Biosciences and the Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff CF10 3AX, United Kingdom.
Proceedings of the National Academy of Sciences (Impact Factor: 9.67). 01/2012; 109(4):1311-6. DOI: 10.1073/pnas.1112204109
Source: PubMed


Ocular dominance (OD) plasticity in the visual cortex is a classic model system for understanding developmental plasticity, but the visual cortex also shows plasticity in adulthood. Whether the plasticity mechanisms are similar or different at the two ages is not clear. Several plasticity mechanisms operate during development, including homeostatic plasticity, which acts to maintain the total excitatory drive to a neuron. In agreement with this idea, we found that an often-studied substrain of C57BL/6 mice, C57BL/6JOlaHsd (6JOla), lacks both the homeostatic component of OD plasticity as assessed by intrinsic signal imaging and synaptic scaling of mEPSC amplitudes after a short period of dark exposure during the critical period, whereas another substrain, C57BL/6J (6J), exhibits both plasticity processes. However, in adult mice, OD plasticity was identical in the 6JOla and 6J substrains, suggesting that adult plasticity occurs by a different mechanism. Consistent with this interpretation, adult OD plasticity was normal in TNFα knockout mice, which are known to lack juvenile synaptic scaling and the homeostatic component of OD plasticity, but was absent in adult α-calcium/calmodulin-dependent protein kinase II;T286A (αCaMKII(T286A)) mice, which have a point mutation that prevents autophosphorylation of αCaMKII. We conclude that increased responsiveness to open-eye stimulation after monocular deprivation during the critical period is a homeostatic process that depends mechanistically on synaptic scaling during the critical period, whereas in adult mice it is mediated by a different mechanism that requires αCaMKII autophosphorylation. Thus, our study reveals a transition between homeostatic and long-term potentiation-like plasticity mechanisms with increasing age.

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Available from: Claire E J Cheetham
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    • "Inhibition of MMPs prevented experience-induced adult visual cortex plasticity MMPs were shown to be critical for open eye potentiation after 7 days of MD in juvenile rats (Spolidoro et al., 2012). Since it is believed that the mechanisms underlying juvenile and adult ODplasticity are different (Hofer et al., 2006; Sato and Stryker, 2008; Ranson et al., 2012), we aimed to test whether MMPs also play a significant role in adult V1-plasticity, in which open-eye potentiation is a major component mediating these changes. First, we induced 7-day-MD in 3-month-old mice and examined whether treatment with GM6001 (50mg/kg/day, for 7days), a broad-spectrum MMP-inhibitor, can prevent ocular dominance (OD) plasticity, measured by in vivo intrinsic signal optical imaging in V1. Figure 1 shows representative examples of optically recorded activity and polar maps after visual stimulation of the right (deprived, contralateral) and left (open, ipsilateral) eye in the binocular region of the left V1 in vehicle-treated (control, Figure 1A,C) and GM6001- treated adult mice (GM6001, Figure 1B,D). "
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