QUANTITATIVE LOCALIZATION OF AMPA KAINATE AND KAINATE GLUTAMATE-RECEPTOR SUBUNIT IMMUNOREACTIVITY IN NEUROCHEMICALLY IDENTIFIED SUBPOPULATIONS OF NEURONS IN THE PREFRONTAL CORTEX OF THE MACAQUE MONKEY

Excitatory amino acid transmission has been proposed as the principal synaptic mechanism for distribution of information through corticocort ical and thalamocortical pathways. The following study utilized a doub le labeling paradigm, using antibodies that recognize non-NMDA ionotro pic glutamate receptor subunits and other neuronal markers, to further define, quantitatively, the subclasses of neurons that contain immuno reactivity for the AMPA/kainate and kainate receptor subunits in the m onkey prefrontal cortex. Double labeling with an antibody that recogni zes common epitopes in AMPA/kainate subunits GluR2 and GluR3 (GluR2/3) in combination with an antibody that recognizes the kainate receptor subunits GluR5, GluR6, and GluR7 (GluR5/6/7) demonstrated that immunor eactivity for these two receptor classes was highly colocalized in a g reat majority of the pyramidal neurons in this region but present in o nly a minority of neurochemically identified subclasses of GABAergic i nterneurons. Furthermore, GluR2/3 immunoreactivity had principally a s omatic distribution whereas GluR5/6/7 labeling was predominately found in the perikarya and/or particular dendritic domains. In contrast, in tense GluR1 labeling was observed in a small subpopulation of interneu rons and low GluR1 immunoreactivity was present in many other cortical neurons. These results demonstrate that there is a high degree of spe cificity in the distribution of AMPA/kainate and kainate receptor-clas s proteins to subclasses of neurons within the neocortex. A neuron's c ombination of excitatory amino acid receptor subunits may regulate its response to excitatory inputs and further defines the role of identif ied subclasses of neurons in the complex circuitry of the cerebral cor tex and may also indicate the basis for the apparent cellular selectiv ity of excitotoxic degenerative processes.