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Abstract

Neuron proliferation in the hippocampus of Prozac-treated homozygous leaner and wild type mice

Summary

The tottering and leaner mutations in mice cause decreases in calcium current through neuronal P/Q-type high voltage calcium channels and neuronal intracellular calcium ion homeostasis is affected by both the leaner and tottering mutations.  Changes in intracellular calcium homeostasis could affect neuronal function and/or survival in these mutant mice, leading to fewer than normal neurons in the hippocampus of these mutant mice.  Both homozygous tottering and homozygous leaner mice have lower forebrain weights compared to age-matched wild type mice. We examined the number of nuclei that incorporated bromodeoxyuridine (BrdU) in the subgranular zone of the dentate gyrus of the hippocampus in homozygous tottering and leaner mice that were given Prozac in lactated Ringer's solution or lactated Ringer's solution only.  We also compared the incorporation rate of BrdU into nuclei in Prozac-treated and vehicle-treated wild type mice.  We observed increased numbers of nuclei that incorporated BrdU after Prozac treatment in wild type mice but not in tottering mice.  There was a tendency for increased proliferation in Prozac-treated leaner mice but this increase was not significant, given the sample size that was obtained thus far in the project. Fewer BrdU labeled nuclei were observed in both leaner and tottering mice, when compared to the wild type mice.  Double labeling of cells with BrdU and Neuronal protein N, which is a protein that is expressed in all neurons, was initiated and these studies are ongoing.