Quantitative evidence for increase in galanin-immunoreactive terminals in the hippocampal formation following entorhinal cortex lesions in the adult rat

The projection from the entorhinal cortex to the dentate gyrus and hippocampus is severely affected in Alzheimer's disease and there is a depletion of cholinergic terminals but an upregulation of the neuropeptide galanin, which inhibits the release of acetylcholine. Evidence for changes to galanin-immunoreactive terminals in the hippocampal formation was therefore examined after unilateral entorhinal cortex lesions in the adult rat. An increase in the density of galanin-immunoreactive terminals on the lesioned side was evident in the stratum lacunosum moleculare of the hippocampus and the outer molecular layer of the dentate gyrus at 17 days post-lesion, and it increased gradually until the last time point examined, at 40 days post-lesion. Thus we demonstrate that there is an increase in galanin-immunoreactive terminals in the hippocampal formation following entorhinal cortex lesions.