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

Ranson, Adam ORCID: https://orcid.org/0000-0002-4804-0832, Cheetham, Claire E., Fox, Kevin Dyson ORCID: https://orcid.org/0000-0002-2563-112X and Sengpiel, Frank ORCID: https://orcid.org/0000-0002-7060-1851 2012. Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity. Proceedings of the National Academy of Sciences 109 (4) , pp. 1311-1316. 10.1073/pnas.1112204109

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Abstract

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 (αCaMKIIT286A) 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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences Neuroscience and Mental Health Research Institute (NMHRI)
Subjects:	Q Science > QH Natural history > QH301 Biology
Publisher:	National Academy of Sciences
ISSN:	0027-8424
Funders:	MRC
Last Modified:	10 Feb 2024 02:18
URI:	https://orca.cardiff.ac.uk/id/eprint/32183

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