Fig.5.

Cholinergic regulation of anxiety-like behavior. (A) Scopolamine increased novelty-induced hypophagia (NIH) in WT, but not in p75^NTR-/-. (B) Compared to its inactive enantiomer ((+) phenserine), the acetylcholinesterase inhibitor (-) phenserine decreased NIH in WT animals, but had no effect in p75^NTR-/-. (C) p75^NTR deletion causes changes in extracellular ACh levels in hippocampal CA3. In vivo microdialysate measurements were obtained in 15 min increments, with four baseline measurements obtained before animals were exposed to 30 mins of elevation stress. Differences between genotypes were significant by student’s t-test at each individual point (-45min:P=0.0029, -30min:P=0.0034, -15min:P=0.0003, 0min:P=0.0001, 15min:P=0.0416 and +30min:P=0.0101). A highly significant interaction was found between enotype and time (P<0.001) (D) Effects of cholinergic signaling on post-stress anxiety levels. Elevation stress led to a significant decrease in saline treated animals (P=0.0013). Administration of (-)-phenserine leads to an increase in anxiety-like behavior following elevation stress (P=0.009). Elevation stress does not affect latency times in scopolamine treated animals (P=0.1034). (E) Elevation stress causes an acute decrease in NIH latency that can be regulated by LTD blockade. This effect was significantly blocked in animals that have been injected with GluA2_3Y peptide. (F) Intrahippocampal infusion of the GluA2_3Y peptide increases latency response times following stress exposure.