Medial septal cholinergic neurons express c-Jun but do not undergo DNA fragmentation after fornix-fimbria transections

Astrocyte Protection of Neurons

“…Our observation of a protective role for c-Jun in GT1-7 neurons in serum deprivation conditions is consistent with a similar protective role suggested for c-Jun during cerebral ischemia based on the finding of c-Jun induction in resistant dentate gyrus cells and CA3 pyramidal cells, which survive the hypoxic-ischemic insult (57,58). A similar c-Jun induction and correlation with survival has also been recently observed in axotomized medial septal neurons that survive fornix fimbria transection (59). The present study thus adds to a growing literature of a potential beneficial role of c-Jun in stress/injury situations.…”

“…51, 55, and 56). Along these lines, it is only recently that appreciation of the potential survival and regenerative actions of c-Jun have emerged to the forefront and begun to be fully appreciated (19,20,(57)(58)(59)(60)(61)(62)(63)(64)(65)(66)(67)(68). It has been suggested that type, strength, and duration of injury stimulus may determine whether a protective or death-promoting action of c-Jun is observed in a cell.…”

c-Jun mediates axotomy-induced dopamine neuron death in vivo

“…This finding, however, is inconsistent with the role proposed for c-Jun in medial septal neurons (MSN) after transection of the fimbria-fornix (44). Whereas SNc neurons degenerate within weeks after axotomy (14), MSN neurons may survive for an extended period before dying (10,11,30). The disparity in rates of survival in these two populations of CNS neurons may be related to the induction of IEG expression in the axotomized neurons.…”

“…For instance, whereas axotomy of MSN elicits sustained expression of c-Jun, these neurons do not display prolonged expression of other numerous leucine zipper-containing proteins, which are clearly expressed after MFB axotomy (6). This induction of a variety of potential activator protein-1 binding partners in SNc neurons after MFB axotomy may lead to death signals not robustly activated in MSN neurons (11). Whereas the downstream effects of c-Jun activation, which mediate axotomy-induced injury, are unknown, several groups have identified c-Jun in the regulation of several target genes linked to cell death pathways, including the proapoptotic Bcl-2 member BIM (50, 51), the tumor suppressor p53 (52), and cyclin D1 (53,54).…”

Polymorphisms of Estrogen Biosynthesis and Metabolizing Genes in Egyptian Women With Breast Cancer.

“…COMT activity is found highly in kidney and liver, and it is also present at high levels in RBCs, brain, the mammary gland and uterine endometrium. The COMT gene, found on 22q11.1-q11.2 chromosome, has a G>A single-nucleotide polymorphism in codon 158/108 of the membrane bound/cytosolic form (Butterworth , Dragunow, 1996). It causes an amino acid change, Val>Met , which determining high-and low-activity alleles of the enzyme (Lachman, et al;.…”