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Publication : Steel mutant mice are deficient in hippocampal learning but not long-term potentiation.

First Author  Motro B Year  1996
Journal  Proc Natl Acad Sci U S A Volume  93
Issue  5 Pages  1808-13
PubMed ID  8700840 Mgi Jnum  J:32130
Mgi Id  MGI:79635 Doi  10.1073/pnas.93.5.1808
Citation  Motro B, et al. (1996) Steel mutant mice are deficient in hippocampal learning but not long-term potentiation. Proc Natl Acad Sci U S A 93(5):1808-13
abstractText  Mice carrying mutations in either the dominant white-spotting (W) or Steel (Sl) loci exhibit deficits in melanogenesis, gametogenesis, and hematopoiesis. W encodes the Kit receptor tyrosine kinase, while Sl encodes the Kit ligand, Steel factor, and the receptor-ligand pair are contiguously expressed at anatomical sites expected from the phenotypes of W and Sl mice. The c-kit and Steel genes are also both highly expressed in the adult murine hippocampus: Steel is expressed in dentate gyrus neurons whose mossy fiber axons synapse with the c-kit expressing CA3 pyramidal neurons. We report here that Sl/Sld mutant mice have a specific deficit in spatial learning. These mutant mice are also deficient in baseline synaptic transmission between the dentate gyrus and CA3 but show normal long-term potentiation in this pathway. These observations demonstrate a role for Steel factor/Kit signaling in the adult nervous system and suggest that a severe deficit in hippocampal-dependent learning need not be associated with reduced hippocampal long-term potentiation.
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