Coons KD, Munoz F, Osborne MC, Sengelaub DR (2009) Dendritic atrophy following partial motoneuron depletion: Time course of recovery and protection with androgens and estrogens. Neuroscience 2009 Abstracts 743.2/R17. Society for Neuroscience, Chicago, IL.
Summary: We have previously demonstrated that partial depletion of motoneurons innervating the quadriceps muscles induces dendritic atrophy and loss of function in remaining motoneurons. Furthermore, treatment with testosterone is neuroprotective, and dendritic atrophy and loss of function following partial motoneuron depletion are attenuated in a dose-dependent fashion, and in both male and female rats. In the present study, we assessed dendritic atrophy after partial motoneuron depletion at a variety of time points to determine its time course and pattern with and without testosterone treatment. We also examined the potential neuroprotective effects of the androgenic and estrogenic metabolites of testosterone. Motoneurons innervating the vastus medialis muscle were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, saporin-injected males were given implants containing either testosterone (45mm), dihydrotestosterone (30mm), estradiol (10%, 10mm), or left untreated. At 2, 4, 6, or 10 weeks after partial motoneuron depletion, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. Animals treated with dihydrotestosterone or estradiol were assessed only at 4 weeks post depletion. Dendritic arbors were also assessed in a group of untreated normal males. Quadriceps motoneuron dendrites underwent a rapid atrophy and protracted recovery following partial motoneuron depletion. Dendritic atrophy in remaining quadriceps motoneurons was apparent at 2 weeks after motoneuron depletion, with a decrease of over 50% in dendritic length, and this atrophy remained through 6 weeks post-depletion; dendritic length recovered by 10 weeks post-depletion. Treatment with testosterone attenuated induced dendritic atrophy at all time points, and recovery to normal lengths was present at 6 weeks post-depletion. Treatment with dihydrotestosterone or estradiol was as effective as testosterone in attenuating dendritic atrophy in remaining quadriceps motoneurons. These results suggest that treatment with testosterone is neuroprotective, both attenuating induced dendritic atrophy and accelerating recovery. Furthermore, this effect can be achieved with both androgenic and estrogenic metabolites, further supporting a role for hormones as neurotherapeutic agents in the injured nervous system.
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