Abstract

To understand the molecular and cellular bases of plasticity in the primate motor cortex, we investigated the expression of three protein kinase-C (PKC) substrates: GAP-43, myristoylated alanine-rich C-kinase substrate (MARCKS), and neurogranin, which are key molecules regulating synaptic plasticity. Prominent signals for the three mRNAs were primarily observed in pyramidal cells. Large pyramidal cells in layer V, from which the descending motor tract originates, contained weaker hybridization signals for GAP-43 and neurogranin mRNAs than did the smaller pyramidal cells. We also performed double-label in situ hybridization showing that GAP-43 and neurogranin mRNAs were expressed in a subset of MARCKS-positive neurons. Quantitative analysis showed that the expression was different between the layers: layer VI contained the strongest and layer II the weakest signals for all three mRNAs. The expression levels of GAP-43 and MARCKS mRNA in layer V were higher than in layer III, while the expression level of neurogranin mRNA in layer V was almost the same as in layer III. Developmental analysis from the newborn to adult indicated that the expression levels of the three mRNAs were higher in the infant motor cortex than in the adult. The expression of both GAP-43 and neurogranin mRNAs transiently increased over several months postnatally. The present study showed that the expression of the three PKC substrates was specific to cell types, cortical layers, and postnatal developmental stage. The specific expression may reflect functional specialization for plasticity in the motor cortex of both infants and adults.

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