A.W. Lyckman1,2,3*; S.H. Horng2,3; S. Oray2,3; M. Sur2,3
1. Neurology, Caritas St. Elizabeth's Medical Center, Boston, MA, USA 2. Picower Center for Learning & Memory, 3. Brain & Cognitive Sciences, MIT, Cambridge, MA, USA

Ocular dominance plasticity (ODP) in the developing visual cortex is a model of activity-dependent cortical synaptic plasticity. Calcium appears to be a key signaling molecule in this system. Here, we show that cardiac troponin C (CTC), an EF-hand calcium-binding protein typically associated with regulation of actin-myosin interactions in heart muscle, may have a prominent role in mediating ODP. CTC mRNA is strongly upregulated in mouse visual cortex at the peak of ODP, as demonstrated by both DNA microarray analysis and semi-quantitative PCR. Immunofluorescence shows that CTC protein is widely expressed throughout the early postnatal mouse brain, but becomes largely restricted to layer IV cortical excitatory neurons by P15. CTC protein levels fall in response to brief (3d) monocular deprivation during the critical period for ODP. CTC in layer IV neurons is largely nuclear or perinuclear suggesting that it transits between the nucleus and cytoplasm. Western blotting shows that heart and cortex coexpress isoforms of 50 and 25kD, while isoforms of 18kD and 41kD are specific to heart and cortex, respectively. These data demonstrate the discovery of a layer IV specific calcium-binding regulatory protein whose expression is development- and activity-dependent, and that is potentially involved in physiological and structural synaptic plasticity during the critical period.
Support Contributed By: NIH grants EY14134 and EY15068