| First Author | Beck RD Jr | Year | 2005 |
| Journal | J Neuroimmunol | Volume | 160 |
| Issue | 1-2 | Pages | 146-53 |
| PubMed ID | 15710467 | Mgi Jnum | J:101962 |
| Mgi Id | MGI:3605966 | Doi | 10.1016/j.jneuroim.2004.11.006 |
| Citation | Beck RD Jr, et al. (2005) IL-2 deficiency results in altered septal and hippocampal cytoarchitecture: relation to development and neurotrophins. J Neuroimmunol 160(1-2):146-53 |
| abstractText | We have found previously that brain IL-2 receptors are enriched in the hippocampal formation, and that loss of this cytokine results in cytoarchitectural alterations in the hippocampus and septum and related behavioral changes in IL-2 knockout (IL-2 KO) mice. These alterations included decreased cholinergic somata in the medial septum/vertical limb of the diagonal band of Broca (MS/vDB) and decreased distance across the infrapyramidal (IP) granule cell layer (GCL) of the dentate gyrus (DG). To extend our previous findings, several experiments were conducted comparing IL-2 KO mice and wild-type littermates to determine (1) whether the GABAergic projection neurons of IL-2 KO mice in this region were also affected; (2) if the reduction in septal cholinergic projection neurons found in adult IL-2 KO mice is present at weaning (and prior to the development of peripheral autoimmune disease); and (3) if loss of IL-2 may result in changes in the neurotrophins, brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), involved in maintenance of hippocampal neurons. No differences in GABAergic neurons in the MS/vDB were found in adult mice, and the reduction in cholinergic neurons seen in adult IL-2 KO mice was not found in animals at postnatal day 21. The number of neurons in the IP-GCL was also significantly reduced. Compared to wild-type mice, IL-2 KO mice had significantly reduced concentration of BDNF protein and increased concentrations of NGF. These data suggest that the septohippocampal neuronal loss in IL-2 KO mice is selective for the cholinergic neurons and appears to be due to a failure in neuronal maintenance/survival that may be, in part, associated with changes in neurotrophins. |
