Ferguson AS, Sengelaub DR (2007) Dendritic atrophy following partial motoneuron depletion: time course of recovery and protection with testosterone. Neuroscience 2007 Abstracts 56.24/S18. Society for Neuroscience, San Diego, CA.
Summary: In male rats, motoneurons of the spinal nucleus of the bulbocavernosus (SNB) project to the bulbocavernosus and levator ani (BC/LA) muscles, and both the motoneurons and their target muscles are highly androgen-sensitive. We have previously demonstrated that partial depletion of motoneurons from the SNB induces dendritic atrophy in remaining motoneurons, and that treatment with testosterone (T) is neuroprotective against this atrophy. In the present study, we assessed dendritic atrophy after partial motoneuron depletion in SNB motoneurons at a variety of time points, to determine its time course and pattern with and without T treatment. Motoneurons innervating the BC/LA muscles in gonadally intact males were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, saporin-injected males were given T implants (45mm) or left untreated. At 2, 4, 6, or 10 weeks after motoneuron depletion, motoneurons innervating the contralateral BC were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. As previously reported, partial motoneuron depletion resulted in dendritic atrophy in remaining SNB motoneurons. While motoneuron depletion occurs within 7 days after saporin injection, dendritic atrophy in remaining SNB motoneurons progresses linearly over several weeks, with a decrease of 32% present at 2 weeks after motoneuron depletion, and a decrease to 66% at 4 weeks. Evidence of recovery in dendritic lengths was observed at 6 weeks post depletion (only 43% decreased), and by 10 weeks SNB dendritic lengths had returned to those of normal, intact males. Treatment with T altered the pattern of dendritic atrophy. While initial dendritic atrophy was similar to that of untreated saporin-injected males (29% decreased at 2 weeks post motoneuron depletion), T treatment attenuated dendritic atrophy. Four weeks after motoneuron depletion, SNB dendritic lengths had not declined further in T-treated males (32% decreased), and were now 102% longer than those of untreated, saporin-injected males. These findings suggest that SNB dendrites undergo a protracted atrophy and subsequent recovery following partial motoneuron depletion, and that the neuroprotective effects of T attenuate the magnitude of the induced atrophy.
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