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The Journal of Neuroscience, October 13, 2004, 24(41):9049-9058; doi:10.1523/JNEUROSCI.2409-04.2004

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Development/Plasticity/Repair
Requirement for the RII Isoform of PKA, But Not Calcium-Stimulated Adenylyl Cyclase, in Visual Cortical Plasticity

Quentin S. Fischer,¹ Christopher J. Beaver,¹ Yupeng Yang,¹ Yan Rao,¹ Klara B. Jakobsdottir,¹ Daniel R. Storm,² G. Stanley McKnight,² and Nigel W. Daw¹

¹Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut 06520, and ²Department of Pharmacology, University of Washington School of Medicine, Seattle, Washington 98195

The cAMP-dependent protein kinase (PKA) signaling pathway plays a key role in visual cortical plasticity. Inhibitors that block activation of all PKA regulatory subunits (RI,RI, RII, RII) abolish long-term potentiation (LTP) and long-term depression (LTD) in vitro and ocular dominance plasticity (ODP) in vivo. The details of this signaling cascade, however, including the source of PKA signals and which PKA subunits are involved, are unknown. To investigate these issues we have examined LTP, LTD, and ODP in knock-out mice lacking either the two cortically expressed Ca²⁺-stimulated adenylyl cyclases (AC1 and AC8) or the predominant neocortical subunit of PKA (RII). Here we show that plasticity remains intact in AC1/AC8-/- mice, whereas ODP and LTD, but not LTP, are absent in RII-/- mice. We conclude that (1) plasticity in the visual cortex does not require the activity of known Ca²⁺-stimulated adenylyl cyclases, (2) the PKA dependence of ODP and LTD, but not LTP, is mediated by RII-PKA, and (3) multiple isoforms of PKA contribute to LTD.

Key words: cAMP-dependent protein kinase; LTP; LTD; ocular dominance plasticity; monocular deprivation; visual cortex

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Received June 18, 2004; revised September 5, 2004; accepted September 6, 2004.

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