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Estrogen supports structural plasticity of the basal forebrain cholinergic system in vivo

Saenz C, Dominguez R, de Lacalle S (2004) Estrogen supports structural plasticity of the basal forebrain cholinergic system in vivo. Neuroscience 2004 Abstracts 72.11. Society for Neuroscience, San Diego, CA.

Summary: It is known that estrogen (E2) modulates the structural plasticity of a variety of neurons, involving the activation of second messenger systems. We have previously described a strong E2-induced outgrowth in cholinergic neurons in vitro, and in the present study we follow up those results and examine E2’s ability to enhance cholinergic arborization in vivo, under several conditions. Twenty F344 female rats were used, 10 of them gonadectomized. All the rats received a unilateral lesion (200 nl of 192 IgG-saporin) into the left HDB, and a month later were randomly assigned to receive E2 or placebo via s.c. pellets for 60 days, at which point the rats were sacrificed, the brains prepared for histology and series of sections stained with an antibody against p75NTR. Sections were carefully matched across individuals, 10 neurons selected from both lesioned and intact HDB, and photographed. Neurons were chosen from the same area in all cases, located in the periphery of the HDB, where the neuritic arborization could be easily identified. Image analysis was performed using Metamorph software, on a predetermined set of parameters. Each image was the result of a stack of photographs taken at 2 µm intervals through the depth of the section. We compared mean neurite number per neuron and total neurite length per neuron, and found that in the healthy cholinergic neurons (control side), E2 contributed to a significant increase in neurite length and number. By contrast, no effect was found on cholinergic neurons from the lesioned side, showing that E2 cannot reverse the neuronal degeneration induced by the immunotoxin. These results are important in that they provide additional support to the hypothesis that E2 may be beneficial in preventing cholinergic degeneration, but no longer useful once neuronal damage has occurred.

Related Products: 192-IgG-SAP (Cat. #IT-01)

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