Fargo KN, Sengelaub DR (2004) Prevention of depletion-induced motoneuron dendritic atrophy requires testosterone effects on target musculature. Neuroscience 2004 Abstracts 310.10. Society for Neuroscience, San Diego, CA.
Summary: Motoneurons in the spinal nucleus of the bulbocavernosus (SNB) in male rats project to the penile muscles bulbocavernosus (BC) and levator ani (LA). These motoneurons share a midline location, have intermingled somata, extensive dendritic overlap, and common afferents, and organize coordinated contractions of the penile musculature. Unilateral depletion of BC-projecting motoneurons causes marked dendritic atrophy in contralateral BC-projecting motoneurons, and this atrophy can be prevented with testosterone (T) treatment. In this experiment, we test whether the depletion-induced atrophy is related to the innervation of homotypic muscles. BC-projecting motoneurons were depleted by unilateral injection with saporin conjugated to the cholera toxin B subunit (SAP); some animals were simultaneously treated with T. Four weeks later, a period demonstrated to be sufficient to observe dendritic atrophy in remaining motoneurons, HRP conjugated to the cholera toxin B subunit (BHRP) was injected into the ipsilateral LA. SAP injection into the BC muscle killed over 40% of ipsilateral SNB motoneurons. Dendritic length in LA-projecting motoneurons was reduced by almost 60%. Because the SAP-induced depletion of motoneurons and the resultant dendritic atrophy occurred across motor populations, this result indicates that the dendritic atrophy we have observed previously is not restricted to motoneurons projecting to homotypic muscles. In previous studies, prevention of dendritic atrophy by T treatment in BC-projecting motoneurons was accompanied by a marked hypertrophy of the BC muscle. In the present experiment, T treatment failed to prevent dendritic atrophy in LA-projecting motoneurons, and further did not result in hypertrophy of the LA ipsilateral to the SAP-injected BC. Thus, it appears the neuroprotective effect of T treatment on SNB motoneurons may be dependent on T effects in the target musculature.
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