Dendritic spines are major sites of excitatory synaptic transmission and changes in their densities have been linked to alterations in learning and memory. The neurotrophins brain-derived neurotrophic factor and neurotrophin-3 and their receptors, trkB and trkC, are thought to be involved in learning, memory and long-term potentiation (LTP). LTP is known to induce trkB and trkC gene expression as well as spinogenesis in the hippocampus. In the aging hippocampus, declines in trkB and trkC mRNA levels may underlie, at least in part, impairments in spatial memory and reductions in spine densities. To determine the significance of trkB and trkC for the maintenance of dendritic spines, we have analyzed Golgi-impregnated hippocampi of adult and aged mice heterozygous for trkB, trkC, or both along with respective wildtype littermates. Deletion of one allele of trkB, but not trkC, significantly reduces spine densities of CA1 pyramidal neurons in both adult and aged mice, as compared to age-matched controls. This indicates that trkB, but not trkC, receptors are necessary for the maintenance of hippocampal spines during postnatal life.
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Animals, Dendrites, Hippocampus, Male, Mice, Mice, Inbred Strains, Mice, Knockout, Mice, Transgenic, Receptor, trkB, Receptor, trkC