Steel mutant mice are deficient in hippocampal learning but not long-term potentiation.
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.
Motro
B
B
Program in Molecular Biology and Cancer, Samuel Lunenfeld Reseaerch Institute, Mount Sinai Hospital, Toronto, Canada.
Wojtowicz
J M
JM
Bernstein
A
A
van der Kooy
D
D
D000818:Animals; D006579:Heterozygote; D006624:Hippocampus / Q000502:physiology*; D007858:Learning / Q000502:physiology*; D017774:Long-Term Potentiation / Q000502:physiology*; D051379:Mice; D008817:Mice, Mutant Strains; D015398:Signal Transduction; D019089:Stem Cell Factor / Q000502:physiology*; D009435:Synaptic Transmission
D019089:Stem Cell Factor