Hartonian I, de Lacalle S (2001) Long-term plastic changes in galanin innervation in rat basal forebrain. Neuroscience 2001 Abstracts 254.1. Society for Neuroscience, San Diego, CA.
Summary: Galanin (GAL) immunoreactive (-ir) fibers hyperinnervate remaining cholinergic basal forebrain neurons in Alzheimer’s Disease (AD), perhaps exacerbating the cholinergic deficit. The purpose of our study is to determine whether a similar hyperinnervation of GAL-ir fibers occurs following intraparenchymal injection of 192-IgG saporin, a specific cholinergic neurotoxin, within the horizontal diagonal band of Broca (HDB), in 3-month-old rats, and to identify its origin. Immunotoxic lesions produced on average a 31% reduction in cholinergic cell counts on the lesioned side versus the spared side. Hyperinnervation of GAL-ir fibers was observed within and adjacent to the HDB in 28 out of 36 rats, and this effect persisted across time, with 6 months being the longest time examined. Morphometry revealed an increase in the number of GAL-ir cells on the lesioned basal forebrain, as compared to control. A similar change could not be detected in the number of GAL-ir neurons in the amygdala or the bed nucleus of the stria terminalis. Although there was no significant correlation in the amount of cell loss and of GAL hyperinnervation, we suggest that GAL hyperinnervation is triggered by the loss of cells because it is persistent across time. Our data suggests that this hyperinnervation is the result of overexpression of GAL in some cholinergic neurons of the basal forebrain. Since GAL is known to inhibit acetylcholine release, exacerbating the cholinergic dysfunction in AD, this model can be useful to test the efficacy of GAL inhibitors.
Related Products: 192-IgG-SAP (Cat. #IT-01)