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Activation of NF-κB signaling in the hippocampus without cholinergic input was aggravated by chronic stress

Lee S-Y, Kim M-S, Han J-S (2013) Activation of NF-κB signaling in the hippocampus without cholinergic input was aggravated by chronic stress. Neuroscience 2013 Abstracts 717.18. Society for Neuroscience, San Diego, CA.

Summary: Previous studies have demonstrated that loss of cholinergic input to hippocampus contributes dysfunction of HPA axis and alters GR-PKA-NF-κB signaling in hippocampus. In the hippocampus without cholinergic input, interactions of GR and PKA are decreased, whereas interactions of PKA and NF-κB are increased and phosphorylations on Ser276 of NF-κB p65 are increased. On the other hand, activation of NF-κB p65 is associated with behavioral action of stress and depression. The present research was conducted to examine whether NF-κB activation induced by cholinergic lesions is aggravated in response to chronic stress. Young adult rats received immunotoxic lesions of basal forebrain cholinergic neurons by intracranial injections of 192 IgG-saporin into the medial septum/vertical limb of the diagonal band and substantia innominata/nucleus basalis. After 2 weeks recovery from surgery, rats with cholinergic lesions and vehicle-injected control rats were subjected to 1 hr restraint stress per day for 2 weeks. We examined that cholinergic deafferentation induced alterations in GR and NF-κB p65 expression in hippocampus and prefrontal cortex. Rats with cholinergic deafferentation and chronic stress showed more activation of NF-κB p65 signaling in the hippocampus compared with rats with cholinergic deafferentation only. Thus the loss of cholinergic integrity during aging and in AD might increase proneness to chronic stress.

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