ALPHA CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE-II SELECTIVELY EXPRESSED IN A SUBPOPULATION OF EXCITATORY NEURONS IN MONKEY SENSORY-MOTORCORTEX - COMPARISON WITH GAD-67 EXPRESSION/

In situ hybridization histochemistry and immunocytochemistry, includin g double immunofluorescence, were used to study the populations of neu rons expressing the alpha subunit of type II calcium/calmodulin-depend ent protein kinase (CAM II kinase-alpha) or glutamic acid decarboxylas e (GAD) in the somatic sensory and motor areas of the macaque monkey c erebral cortex. Sections were subjected to in situ hybridization using radioactive, complementary RNA probes specific for monkey CAM II kina se-alpha or 67 kDa GAD mRNAs. Others were stained immunocytochemically for CAM II kinase-cu and/or GABA. CAM II kinase-alpha and GAD-67 are expressed in different populations of cells, with no colocalization. C AM II kinase-alpha is expressed in pyramidal cells of layers II-VI, es pecially layers II and III, as well as in certain small nonpyramidal c ells of layer IV in areas 3a, 3b, 1, and 2 and of middle regions of ar ea 4. Both cell types produce excitatory amino acid transmitters. Ther efore, as in subcortical regions, CAM II kinase-alpha will be found on the presynaptic side of excitatory synapses but on the postsynaptic s ide only when these synapses occur on excitatory neurons in the sensor y-motor cortex. Quantitative examination showed that CAM II kinase-alp ha immunoreactive cells form, on average, approximately 50% of the tot al neuronal population in each area, while GABA immunoreactive or GAD cRNA hybridized cells form approximately 25-30%. Thus, CAM II kinase-a lpha expressing cells cannot account for the total population of non-G ABAergic cortical cells, and a certain proportion of the pyramidal cel ls probably do not express it. In other cortical areas, gene expressio n for the two molecules is regulated by afferent activity. Therefore, the present results form a necessary basis for studies aimed at determ ining the role of activity-dependent changes in the balance of excitat ion and inhibition as a mechanism underlying plasticity of representat ional maps in the primate sensory-motor cortex.