Elsevier

Experimental Neurology

Volume 161, Issue 1, January 2000, Pages 227-233
Experimental Neurology

Regular Article
Is Fos Protein Expressed by Dying Striatal Neurons after Immature Hypoxic–Ischemic Brain Injury?

https://doi.org/10.1006/exnr.1999.7248Get rights and content

Abstract

The transient induction of mRNA for the immediate–early gene c-fos has been reported following hypoxic–ischemic brain injury in the immature brain. However, no studies have examined the temporal expression of Fos protein, which is the functionally relevant product of c-fos gene expression. Increased expression of Fos protein has been linked to cell death. We therefore examined whether Fos protein is expressed by dying neurons after immature hypoxic–ischemic brain injury. A well characterized immature rat model of hypoxic–ischemic injury at postnatal day (PN) 7 was used. Three hypoxic–ischemic and three normoxic control pups were studied per time point (i.e., 0, 2, 12, 24, 48, and 72 h posttreatment). Expression of Fos within striatal and other neurons was detected immunocytochemically. Fos protein was expressed within dying striatal neurons at 0–12 h after hypoxia–ischemia. However, detection was only seen in 2 of 17 hypoxic–ischemic pups. These 2 pups had ≥80% of their striatal neurons dying within their right, hypoxic–ischemic-exposed hemisphere. Fos protein expression after severe injury may, therefore, be a response to extraordinary or extreme stress. The absence of Fos protein expression in the majority of hypoxic-ischemic pups, which all exhibited striatal neuronal death, suggests that Fos expression is not necessary for cell death to occur. Therapies directed against Fos protein expression may therefore have limited usefulness in immature hypoxic–ischemic brain injury.

References (34)

Cited by (15)

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    There is also an increased expression of endogenous bFGF after injury to the cerebral cortex and striatum [19,20]. Thus, bFGF treatment that is delayed after hypoxic–ischemic injury may take over from the endogenous bFGF response and prevent the neuronal degeneration that normally ensues during at least the first 72 h after perinatal hypoxic–ischemic injury [21,22]. Therefore, the aim of this study was to determine the effect of delayed treatment with bFGF on neuronal survival within the rat striatum after immature hypoxic–ischemic brain injury.

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    Instead a robust expression of c-Fos was observed in the ventricular/intermediate zone. The expression of c-Fos or of the c-Fos related antigen-2 might occur in degenerating neurons as well as in neurons surviving excitotoxic or hypoxic insults (Tong and Perez-Polo, 1998; Franke et al., 2000; Oorschot et al., 2000; Pennypacker et al., 2000). The involvment of c-Fos in either process critically depends on the developmental state, on the neurotrophin dependency and on the intracellular signaling machinery active in a given neuron.

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Current address: Rebecca L. Cooper Research Laboratories, The Mental Health Research Institute of Victoria, Locked Bag 11, Parkville, Victoria, 3052 Australia.

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