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Reduced ocular dominance plasticity and long‐term potentiation in the developing visual cortex of protein kinase A RIIα mutant mice
Author(s) -
Rao Yan,
Fischer Quentin S.,
Yang Yupeng,
McKnight G. Stanley,
LaRue Adrienne,
Daw Nigel W.
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03499.x
Subject(s) - monocular deprivation , long term potentiation , visual cortex , ocular dominance , neuroscience , protein subunit , biology , synaptic plasticity , knockout mouse , neuroplasticity , protein kinase a , plasticity , microbiology and biotechnology , kinase , receptor , genetics , physics , thermodynamics , gene
The cAMP‐dependent protein kinase (PKA) signalling pathway has been shown to play an important role in long‐term potentiation (LTP) and depression (LTD), and ocular dominance plasticity in the visual cortex. In order to investigate further the involvement of individual PKA subunits in visual cortical plasticity , LTP and LTD in vitro and ocular dominance plasticity in vivo in the developing visual cortex were examined in mice lacking the RIIα subunit of PKA. Here we show that LTP in layers II/III was decreased in RIIα knockout mice, but LTD was almost unaffected, and the ocular dominance shift induced by monocular deprivation was also partially blocked. These data provide evidence that RIIα is involved in LTP and ocular dominance plasticity, and further suggest that different afferent inputs could selectively activate particular subunits of PKA and thereby direct specific aspects of visual cortical plasticity.