N--methyl-d-aspartate receptors mediate activation of the c-fos proto-oncogene in a model of brain injury
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Cited by (104)
Deregulation of NMDA-receptor function and down-stream signaling in APP[V717I] transgenic mice
2009, Neurobiology of AgingCitation Excerpt :In hippocampus and amygdala the immediate early gene c-Fos is induced following training in a variety of learning tasks (Miyamoto, 2006; Tischmeyer and Grimm, 1999), while c-Fos deficiency impairs memory (Fleischmann et al., 2003). Several studies demonstrated association between NMDA-receptor activity and c-Fos regulation in different models of synaptic plasticity (Cole et al., 1989; Herrera and Robertson, 1990; Aronin et al., 1991) as well as in long-term memory formation (Fleischmann et al., 2003; Savonenko et al., 2003) (for reviews, Kaczmarek and Chaudhuri, 1997; Platenik et al., 2000; Kaczmarek, 2002). We here report for the first time decreased concentrations of activated and translocated α-CamkII in postsynaptic densities of APP[V717I] transgenic mice.
Hormesis: A promising strategy to sustain endogenous neuronal survival pathways against neurodegenerative disorders
2008, Ageing Research ReviewsCitation Excerpt :NMDA receptors play a crucial role in the induction of long-term potentiation (LTP) (Herron et al., 1986), a model of learning and memory. NMDA receptor activation increases the synthesis of immediate early genes (IEGs) (Cole et al., 1989; Hughes et al., 1993; Herrera and Robertson, 1990a,b; Herrera et al., 1992) and NMDA receptors coordinate a protection program in neurons that requires the release and synthesis/release of BDNF. Nuclear factor kappa B (NF-κB) is a ubiquitously expressed transcription factor that plays a key role in diverse cellular processes, including adaptive immune responses, stress responses, cell survival and proliferation (Baldwin, 1996; Karin, 1999).
Regional expression of constitutive and inducible transcription factors following transient focal ischemia in the neonatal rat: Influence of hypothermia
2005, Brain ResearchCitation Excerpt :Spreading depression is confined to the ipsilateral hemisphere, where it influences the volume of focal ischemic damage [5]. The classic induction of spreading depression by KCl application has been associated with a similar pattern of c-Fos expression to that observed in adult focal ischemia models [24]. In contrast to what is observed in adults, c-fos induction in P7 rats is initially expressed in a thin boundary surrounding the ischemic infarct and hence does not appear to be related to spreading depression.
Inhibition of calpain-mediated apoptosis by E-64 d-reduced immediate early gene (IEG) expression and reactive astrogliosis in the lesion and penumbra following spinal cord injury in rats
2001, Brain ResearchCitation Excerpt :Also, an increase in c-fos expression has been reported in traumatic brain injury [58] and is found to be associated with neuronal apoptosis [18,72]. Increased expression of both c-jun and c-fos has been reported in experimental models of brain ischemia [49] and brain trauma [19,30]. Our investigation reveals that mRNA expression of c-jun (Fig. 4) and c-fos (Fig. 5) are also increased at various levels in the lesion and penumbra following SCI in rats.
The acetylcholine release enhancer linopirdine induces Fos in neocortex of aged rats
2001, Neurobiology of AgingCitation Excerpt :Activation of glutamatergic neurotransmission in the cerebral cortex results in widespread Fos staining [44,67]. A glutamatergic mechanism involving NMDA receptor activation has been demonstrated for the c-fos induction in the cerebral cortex following pentylenetetrazole administration [61], application of potassium chloride to the surface of the brain [33], and mechanical injury by disruption of the pial surface [33,38]. Activation of glutamatergic transmission in the primary motor cortex by focal injections of the GABA receptor blocker picritoxin produced widespread induction of Fos in neocortex that was completely abolished by MK-801 [7].
C-fos expression in rat brain during heat stress
1999, Journal of Thermal Biology