Induction of Fos protein in a model of closed head injury in rats.
The induction of Fos immunoreactivity in the pyriform cortex and the hippocampal formation after closed head injury was determined and compared to that seen following cortical needle injury in pentobarbital anaesthetized male rats. Robust Fos expression was observed in the ipsilateral pyriform cortex following both types of injury but was observed in the ipsilateral dentate gyrus only following closed head injury. Pretreatment with the NMDA receptor blocker MK-801 eliminated closed head injury induced Fos expression in the pyriform cortex and attenuated that seen in the hippocampus. Similar amounts of Fos expression were observed in urethane anaesthetized lactating and nonlactating rats following closed head injury. No gross behavioural impairments as reflected in body weight gain and locomotor activity were seen in animals subjected to closed head injury. These results demonstrate that as with other forms of brain damage, closed head injury at levels that produce no overt brain lesion nor gross behavioural impairment induce Fos expression in the pyriform cortex and the dentate gyrus which is dependent on the activation of NMDA receptors. Further, this response to brain injury is not modulated by lactation.[1]References
- Induction of Fos protein in a model of closed head injury in rats. Woodside, B., Robinson, B., Amir, S. Brain Res. (1995) [Pubmed]
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