title: BDNF concentrations are decreased in serum and parietal cortex in immunotoxin 192 IgG-Saporin rat model of cholinergic degeneration.
abstract: The neurotrophin brain-derived neurotrophic factor (BDNF) has been extensively studied because of its role in survival, differentiation and function of neurons undergoing degeneration in pathological conditions such as cholinergic neurons in Alzheimer's disease (AD). However, despite these evidences, the role of BDNF in these events is still matter of debate because central and peripheral BDNF levels are often found in opposite direction. Another puzzling factor is represented by pharmacological treatments known to cause alterations of BDNF peripheral levels. Thus, a pivotal issue would be to verify whether brain and serum BDNF changes are interconnected as well as the possibility that different stages of cholinergic degeneration are characterized by different changes in BDNF brain and serum levels. With this in mind in this study we used a rat model of cholinergic degeneration based on intracerebroventricular (i.c.v.) injections of 192 IgG-Saporin and measured brain and serum BDNF concentrations by enzyme-linked immunosorbent assay (ELISA) at 3, 7 and 15days from immunotoxin injection. We found that BDNF levels were reduced in parietal cortex and serum of Saporin-treated rats at 15days from lesion. Moreover, a positive correlation between serum and parietal cortex was observed at 15days from lesion. These alterations were not present at the earlier post-operative time points. In conclusion, this study shows that BDNF levels are reduced in a rat model of cholinergic degeneration and suggests that these alterations may occur at later stages. In addition, a positive correlation between serum and parietal cortex changes is observed. Even if the cause for the relationship between BDNF in serum and this brain region is unknown, these data may help to elucidate the significance of peripheral and central BDNF changes in brain pathological conditions.
authors.affiliation: IRCCS Santa Lucia Foundation, Department of Clinical and Behavioral Neurology, 00179 Rome, Italy. f.angelucci@hsantalucia.it
authors.forename: Francesco
authors.initials: F
authors.lastname: Angelucci
authors.forename: Francesca
authors.initials: F
authors.lastname: Gelfo
authors.forename: Paola
authors.initials: P
authors.lastname: De Bartolo
authors.forename: Carlo
authors.initials: C
authors.lastname: Caltagirone
authors.forename: Laura
authors.initials: L
authors.lastname: Petrosini
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D019208:Brain-Derived Neurotrophic Factor / Q000097:blood / Q000378:metabolism*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D007276:Injections, Intraventricular; D008297:Male; D019636:Neurodegenerative Diseases / Q000097:blood / Q000378:metabolism*; D010296:Parietal Lobe / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011950:Receptors, Cholinergic / Q000378:metabolism*; D054789:Ribosome Inactivating Proteins, Type 1 / Q000008:administration & dosage / Q000494:pharmacology*; D000076985:Saporins
chemical_list: C085696:192 IgG-saporin; D000911:Antibodies, Monoclonal; D019208:Brain-Derived Neurotrophic Factor; D011950:Receptors, Cholinergic; D054789:Ribosome Inactivating Proteins, Type 1; D002795:Choline O-Acetyltransferase; D000076985:Saporins