title: Long-term plastic changes in galanin innervation in the rat basal forebrain.
abstract: Galanin immunoreactive fibers hyperinnervate remaining cholinergic basal forebrain neurons in Alzheimer's disease, perhaps exacerbating the cholinergic deficit. The purpose of our study is to determine whether a similar phenomenon occurs following intraparenchymal injection of 192 IgG-saporin, a specific cholinergic neurotoxin, within the nucleus of the horizontal limb of the diagonal band of Broca. Immunotoxic lesion produced on average a 31% reduction in cholinergic cell counts ipsilateral to the lesion, compared to the contralateral side. Increased galanin immunoreactivity, suggestive of increased fiber density, was observed within and adjacent to the lesion in 28 out of 36 rats, and this effect persisted across time up to 6 months (the longest time examined). We observed a parallel increase in the number of galanin positive neurons ipsilateral to the lesion, compared to the contralateral side. No correlative change could be detected in the number of galaninergic neurons in the amygdala or the bed nucleus of the stria terminalis. There was no statistically significant correlation between the extent of cholinergic cell loss and the increase in galanin immunoreactivity surrounding the lesion. Yet, since both of these changes persist over time, we suggest that galanin plasticity is triggered by neuronal damage. Our model can be useful to test the role that galanin plays in the regulation of acetylcholine and the efficacy of galanin inhibitors as potential therapeutic interventions in Alzheimer's disease.
authors.affiliation: Department of Biological Sciences, California State University, 5151 State University Drive, Los Angeles, CA 90032, USA.
authors.forename: I
authors.initials: I
authors.lastname: Hartonian
authors.forename: E J
authors.initials: EJ
authors.lastname: Mufson
authors.forename: S
authors.initials: S
authors.lastname: De Lacalle
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D002452:Cell Count; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism*; D003714:Denervation; D019004:Galanin / Q000378:metabolism*; D007150:Immunohistochemistry; D000922:Immunotoxins / Q000494:pharmacology; D008297:Male; D009699:N-Glycosyl Hydrolases; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011916:Rats, Inbred F344; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins; D012686:Septal Nuclei / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: C085696:192 IgG-saporin; D000911:Antibodies, Monoclonal; D000922:Immunotoxins; D054789:Ribosome Inactivating Proteins, Type 1; D019004:Galanin; D002795:Choline O-Acetyltransferase; D009699:N-Glycosyl Hydrolases; D000076985:Saporins; D000109:Acetylcholine