Regular ArticleIs Fos Protein Expressed by Dying Striatal Neurons after Immature Hypoxic–Ischemic Brain Injury?
References (34)
- et al.
Changes in c-fos mRNA in the neonatal rat brain following hypoxic ischemia
Neurosci. Lett.
(1994) - et al.
Relative loss of the striatal striosome compartment, defined by calbindin-D28K immunostaining, following developmental hypoxic–ischemic injury
Neuroscience
(1993) - et al.
Identification of necrotic cell death by the TUNEL assay in the hypoxic–ischemic neonatal rat brain
Neurosci. Lett.
(1997) - et al.
Dexamethasone prevents apoptosis in a neonatal rat model of hypoxic-ischemic encephalopathy (HIE) by a reactive oxygen species-independent mechanism
Brain Res.
(1997) - et al.
The temporal evolution of striatal dopamine receptor binding and mRNA expression following hypoxia-ischemia in the neonatal rat
Dev. Brain Res.
(1996) - et al.
c-Fos is not essential for apoptosis
Biochem. Biophys. Res. Commun.
(1996) - et al.
The effects of hypoxia-ischemia on expression of c-Fos, c-Jun and Hsp70 in the young rat hippocampus
Mol. Brain Res.
(1997) - et al.
Immediate early gene induction after neonatal hypoxia–ischemia
Mol. Brain Res.
(1993) - et al.
Effects of hypoxia–ischemia and seizures on neuronal and glial-like c-fos protein levels in the infant rat
Brain Res.
(1990) - et al.
Coordinate suppression of striatal ngfi-a and c-fos produces locomotor asymmetry and up-regulation of IEGs in the globus pallidus
Mol. Brain Res.
(1997)
Current concepts of hypoxic–ischemic cerebral injury in the term newborn
Pediatr. Neurol.
DNA fragmentation indicative of apoptosis following unilateral cerebral hypoxia–ischemia in the neonatal rat
Brain Res.
Cell death and associated c-jun induction in perinatal hypoxia–ischemia. Effect of the neuroprotective drug dexamethasone
Mol. Brain Res.
Localization of c-fos, c-jun, and hsp70 mRNA expression in brain after neonatal hypoxia-ischemia
Dev. Brain Res.
Are you using neuronal densities, synaptic densities or neurochemical densities as your definitive data? There is a better way to go
Prog. Neurobiol.
Permanent increase of the GAD67/synaptophysin ratio in rat cerebral cortex nerve endings as a result of hypoxic–ischemic encephalopathy sustained in early postnatal life: A confocal laser scanning microscope study
Brain Res.
Cited by (15)
Effects of short-duration electromagnetic radiation on early postnatal neurogenesis in rats: Fos and NADPH-d histochemical studies
2011, Acta HistochemicaCitation Excerpt :In this study, the cells expressing Fos protein appear mainly to be dying neurons within the striatum, cerebral cortex, medial habenula, and dentate gyrus. Oorschot et al. (2000) reported the detection of Fos protein expression from 0 to 24 h post-injury in P7 rats and this is consistent with other studies (Nozaki and Beal, 1992; Åden et al., 1994; Macaya et al., 1998). Our latest study (Lievajová et al., in press) has demonstrated that stressful experience (maternal deprivation) imposed on P1–P7 rats induces a decrease in proliferating cell numbers and causes premature occurrence and differentiation of NO producing cells within the RMS.
A modified rat model of neonatal anoxia: Development and evaluation by pulseoximetry, arterial gasometry and Fos immunoreactivity
2011, Journal of Neuroscience MethodsEffect of delayed treatment with basic fibroblast growth factor on the survival of striatal spiny projection neurons after perinatal hypoxia–ischemia
2003, International Congress SeriesCitation Excerpt :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.
Developmentally induced microencephalopathy in guinea pigs -embryonic glial cell activation marks selective neuronal death
2001, International Journal of Developmental NeuroscienceCitation Excerpt :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.
- 1
Current address: Rebecca L. Cooper Research Laboratories, The Mental Health Research Institute of Victoria, Locked Bag 11, Parkville, Victoria, 3052 Australia.