Fargo KN, Sengelaub DR (2005) Testosterone treatment prevents deficits in motor activation caused by partial loss of motoneurons. Neuroscience 2005 Abstracts 672.8. Society for Neuroscience, Washington, DC.
Summary: In male rats, motoneurons of the spinal nucleus of the bulbocavernosus (SNB) project to the bulbocavernosus and levator ani muscles (BC/LA). The SNB system is dependent on androgens for its development, adult morphology, and function. We have previously demonstrated that unilateral depletion of SNB motoneurons induces atrophy of dendrites and somata in contralateral SNB motoneurons, and that this atrophy is prevented by treatment with exogenous testosterone. In the present experiment, we tested the hypothesis that this neuroprotective effect of testosterone on the morphology of SNB motoneurons is accompanied by a neuroprotective effect on the electrophysiological function of the system. We unilaterally depleted right-side SNB motoneurons by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, some of the saporin-injected rats were castrated and immediately given exogenous testosterone in subcutaneous Silastic capsules designed to produce testosterone titers in the high-normal physiological range. Four weeks later, animals were anesthetized and spinally transected. A stimulating electrode was placed on the left L6 dorsal root, which carries motor afferents from the BC/LA, and a recording electrode was placed on the motor branch of the left pudendal nerve, which carries SNB motoneuron axons to the BC/LA. Both nerves were then severed distal to electrode placement, and recruitment curves were generated by stimulating through the entire range of effective intensities. Consistent with our previously reported morphological changes, unilateral motoneuron depletion resulted in an attenuation of the recruitment of motoneurons in the contralateral SNB, and this was completely prevented by treatment with exogenous testosterone. This result provides a functional correlate to the neuroprotective effects of testosterone treatment on SNB morphology following unilateral motoneuron depletion, further supporting a role for testosterone as a neurotherapeutic agent in the injured nervous system.
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