In the developing central nervous system, a src-related
protein-tyrosine kinase fyn participates in the myelination process, neuronal growth, and cytoskeletal organization. In adults, fyn has been implicated in learning and memory formation. To test if fyn expression is modulated by neuronal activity, we performed quantitative in situ hybridization (ISH) using brain sections of the adult rats that had undergone either
kainic acid (KA)-induced
seizures or neuronal deafferentation (entorhinal cortex lesion, ECL). In the KA model, a few hours after seizure activities, fyn
mRNA was elevated in the dentate gyrus (DG) (+45%), cerebral cortex layer III (+35%), and piriform cortex (+25%). Conversely, fyn
mRNA consistently decreased in the hippocampal neurons after transection of the major axonal inputs from the entorhinal cortex. Although fyn expression in the brain has been allegedly limited to neurons and oligodendrocytes, we provide in this study the first evidence that fyn
mRNA is highly expressed in the astrocytes involved in reactive
gliosis. In the KA model, the occurrence of fyn-overexpressing astrocytes increased with the progress of neuronal damage in the CA1 and CA3 regions of the hippocampus. In contrast, fyn-overexpressing astrocytes were not observed in the granular cell layer of dentate gyrus (DG), where neurons were not damaged. Likewise, in the ECL model, the most drastic change in fyn
mRNA expression took place at the reactive astrocytes near the
stab wound sites, where fyn
mRNA levels were doubled 4-10 d after the lesion. Collectively, our data suggest that (i) an early induction of fyn
mRNA in neurons is linked to neuronal activity, and (ii) the delayed induction of fyn
mRNA in reactive astrocytes near the damaged cells may play novel signaling roles during glial response.