Neocortex and hippocampus contain distinct distributions of calcium‐calmodulin protein kinase II and GAP43 mRNA

Abstract

Calcium‐calmodulin protein kinase II and GAP43 are two molecules which have been linked to synaptic plasticity. Localization of mRNA for these molecules identifies the neuronal populations which have the potential to utilize these mechanisms. General descriptions for calcium‐calmodulin protein kinase II or GAP43 mRNA have been previously reported. In light of recent evidence that suggests that at some sites these two molecules may interact, we sought to determine the cortical distribution in detail, and to examine the extent of overlap between neuronal populations containing each mRNA. To this end we have used in situ hybridization techniques to study the distribution of calcium‐calmodulin protein kinase II and GAP43 mRNA in adjacent sections of adult rat forebrain. Overall, the distribution patterns were distinct but partially overlapping. For both calcium‐calmodulin protein kinase II and GAP43, mRNA levels were highest in hippocampus, allo‐ and neocortex, compared to moderate to low levels in striatum and thalamic nuclei. Within the heavily labeled regions certain populations expressed both calcium‐calmodulin protein kinase II and GAP43 mRNA at high levels, while other populations were selective for calcium‐calmodulin protein kinase II. In the hippocampus, the stratum pyramidale of CAI‐3 expressed high levels of both calcium‐calmodulin protein kinase II and GAP43 mRNA. Granule cells of the fascia dentata and the stratum radiatum of CA3 both contained moderate to high levels of calcium‐calmodulin protein kinase II mRNA, but near background levels of GAP43 mRNA label. Within the neocortex, deep layers were distinguished from superficial layers by their lack of calcium‐calmodulin protein kinase II mRNA expression within the neuropil, and the presence of GAP43 mRNA in neurons located in layer V and the deepest part of layer VI. Thus, layer V and deep layer VI neurons showed high levels of label for both GAP43 and calcium‐calmodulin protein kinase II mRNA, while neurons of superficial layers contained only calcium‐calmodulin protein kinase II mRNA. These markers differentiate neuronal populations which can also be distinguished on the basis of their ability to undergo specific forms of synaptic plasticity. These different forms of plasticity may be due in part to the laminar‐specific patterns of GAP43 and calcium‐calmodulin protein kinase II mRNA that we have described.