Immediate Early Gene Expression and Delayed Cell Death in Limbic Areas of the Rat Brain after Kainic Acid Treatment and Recovery in the Cold

MyD genes in negative growth control

“…Evidence has been obtained that Egr-1 also trans-activates the p53 promoter, where inhibition of p53 function abrogated Egr-1-dependent apoptosis. Additional evidence for a role for Egr-1 in apoptosis has been obtained in other cell systems as well, including B cell receptor-induced apoptosis in immature B cells (Muthukkuma et al, 1997;Dinkel et al, 1997), apoptosis induced by Ca 2+ ionophor in melanoma cells (Muthukkuma et al, 1995), and stress or growth factor induced apoptosis of neuronal cells (Goodenough et al, 1997;Mesner et al, 1995). The mechanisms by which Egr-1 mediates apoptosis in di erent cell types, including cells of hematopoietic origin, remain to be elucidated.…”

Bile Acid Signaling Is Involved in the Neurological Decline in a Murine Model of Acute Liver Failure

“…Expression and subcellular localization of the described target genes were assessed by real-time PCR, 27 immunoblotting, 28 immunohistochemistry, 29 or immunofluorescence, 28 as previously described.…”

Differential Expression of Egr‐1‐Like DNA‐Binding Activities in the Naive Rat Brain and After Excitatory Stimulation

“…This was reflected by increases in Egr-2 protein expression in both regions and increased Egr-3 immunoreactivity in the hippocampus, with a trend to an increase in the cortex. The protocol of kainic acid administration used in this study leads to increased Egr-1 mRNA, protein, and DNA-binding activity expression in the cortex and hippocampus (Goodenough et al, 1997). In this study, we demonstrate increased Egr-1 DNA-binding activity in the cerebral cortex and hippocampus and variability in the increase observed in the cerebellum.…”

“…1995). Therefore, it is possible that Egr-1 plays a role in the apoptosis that occurs following kainic acid injection in the model used here (Goodenough et al, 1997). Egr-l is also clearly associated with plasticity-related phenomena, such as visual input (Worley et al, 1991), learning (Yau et al, 1996), long-term potentiation (Cole et al, 1989), and resting neuronal activity .…”

“…In each case, control rats received sham treatment with an equivalent volume of PBS. Behavioral changes were recorded until the animals were killed by decapitation at the time of maximum immediate early gene-encoded protein expression: 1 h after the onset of NMDA-induced behaviors, 2 h after pentylenetetrazole injection (Davidson et al, 1996), and 3 h after kainic acid injection (Goodenough et al, 1997). The cerebral cortex, hippocampus, and cerebellum were dissected.…”