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

Protective Effect of Nicotinamide on Neuronal Cells under Oxygen and Glucose Deprivation and Hypoxia/Reoxygenation

“…In animals with middle cerebral arterial occlusion, IEG mRNAs (c-fos, c-jun, nur77 and zif268) were induced in the ipsilateral forebrain, and, less frequently, in the contralateral forebrain, 1, 2 and 3 h after hypoxia [19]. Fos protein was identified in dying striatal neurons after hypoxic-ischemic brain injury [33]. Thus, the reduced hypoxia-induced IEG expression caused by nicotinamide may partially contribute to neuroprotection.…”

A modified rat model of neonatal anoxia: Development and evaluation by pulseoximetry, arterial gasometry and Fos immunoreactivity

“…The first model is hypoxia-ischemia (initially proposed by Levine, 1960), in which seven-day-old rats undergo occlusion of one of the common carotid arteries and are placed in a chamber containing 8% oxygen and 92% nitrogen for periods ranging from 30 min to 3 h (Rice et al, 2004;Gunn et al, 1990;Åden et al, 1994;Vannucci et al, 1999;Oorschot et al, 2000;Ten et al, 2003). The second model is perinatal asphyxia, in which a female about to give birth is decapitated or anesthetized, and its uterus (containing the pups) is removed and immersed in saline solution for 16-25 min (Dell'anna et al, 1995a;Flores et al, 2002;El-Khodor and Boksa, 2003;Cirulli et al, 2003;Juarez et al, 2003;Venerosi et al, 2004).…”

Expression of fos immunoreactivity in some catecholaminergic brainstem neurons in rats following high-altitude exposure

“…In this connection the postnatal rats showed much less Fos immunoreactivity in the NTS and VLM and none in the area postrema at 4,000 m compared to that at 8,000 m. It appears that oxygen‐sensitive peripheral chemoreceptors are not fully developed at birth (Bureau et al, 1985a,b) and hence are activated only in response to very low oxygen tension such as at 8,000 m altitude (severe hypoxia), leading to stimulation of neurons in the NTS and VLM as observed from their expression of Fos immunoreactivity. Fos protein expression in the immature hypoxic‐ischemic brain has been considered as a response to exteme stress (Oorschot et al, 2000). Earlier studies have indicated that response of the carotid chemoreceptors to hypoxia is weak just after birth and that it increases during postnatal development (Sterni et al, 1995, 1999).…”