Expression of c-fos mRNA after cortical ablation in rat brain is modulated by basic fibroblast growth factor (bFGF) and the NMDA receptor is involved in c-fos expression |
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| Institution: | 1. Reeve-Irvine Research Center, University of California, Irvine, United States;2. Department of Anatomy and Neurobiology, University of California, Irvine, United States;3. Department of Neurobiology and Behavior, University of California, Irvine, United States;4. Department of Neurosurgery, University of California, Irvine, United States;5. School of Medicine, University of California, Irvine, United States;1. Reeve-Irvine Research Center University of California Irvine School of Medicine, USA;2. Department of Anatomy & Neurobiology, University of California Irvine School of Medicine, USA;3. Department of Neurobiology & Behavior, University of California Irvine, USA;4. Department of Neurosurgery, University of California Irvine School of Medicine, USA;1. Reeve-Irvine Research Center, University of California at Irvine, 837 Health Sciences Rd., Irvine, CA 92697, USA;2. Department of Anatomy & Neurobiology, University of California at Irvine, Irvine, CA 92697, USA;3. Department of Neurobiology & Behavior, University of California at Irvine, Irvine, CA 92697, USA;4. Department of Neurosurgery, University of California at Irvine, Irvine, CA 92697, USA;5. Center for the Neurobiology of Learning and Memory, University of California at Irvine, Irvine, CA 92697, USA;6. University of California at Irvine School of Medicine, Irvine, CA 92697, USA |
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| Abstract: | Expression of c-fos mRNA after cortical injury was studied using the in situ hybridization technique. Strong signals for c-fos mRNA were observed immediately after cortical ablation in neurons throughout the cortex ipsilateral to the injury. However, this c-fos mRNA expression was transient and disappeared within 6 h after the injury. When basic fibroblast growth factor (bFGF; 1 μg) was applied to the site of ablation, c-fos mRNA signals were observed for a much longer period. Even 24 h after injury, diffuse expression of c-fos mRNA was detected throughout the cortex, being mainly confined to non-neuronal cells. Intraperitoneal injection of MK-801 (3 mg/kg), a non-competitive NMDA receptor antagonist, suppressed the expression of c-fos mRNA after cortical ablation. It suppressed both the immediate and late expression induced by cortical ablation and bFGF. The immediate expression of c-fos in neurons is likely to be due to spreading depression, while neuronal-glial interactions would be involved in the mechanism of late c-fos expression by non-neuronal cells. Our results suggest that induction of c-fos after cortical injury can be modulated by topically applied bFGF and that the N-methyl-d-aspartate (NMDA) receptor is involved in c-fos expression not only caused by injury itself but also induced by injury and bFGF. As the immediate early genes regulate secondary gene responses, the induction of c-fos may contribute to neuronal plasticity and bFGF may enhance its effect. |
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