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Neuroprotective effects of testosterone in two models of spinal motoneuron injury
Author(s) -
Sengelaub Dale R.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.307.4
Subject(s) - axotomy , neuroprotection , testosterone (patch) , neurotrophic factors , endocrinology , neurotrophin , neuroscience , medicine , nerve injury , biology , receptor , central nervous system
Testosterone, a hormone typically associated with sex, aggression, and athletic performance, also has an important role in the maintenance and repair of the nervous system after injury or disease. Following induced death of spinal motoneurons remaining motoneurons atrophy, but this atrophy can be attenuated by treatment with testosterone. Partial motoneuron depletion results in decreased amplitudes of motor nerve activity, and these changes are attenuated by treatment with testosterone, providing a functional correlate to the neuroprotective effects of testosterone treatment on motoneuron morphology. Testosterone also regulates the expression of receptors for trophic factors, proteins critical for the maintenance of normal structure and function. Brain‐derived neurotrophic factor (BDNF) and testosterone have a combinatorial effect in the maintenance of motoneurons after axotomy in that dendritic morphology is supported by BDNF treatment, but only in the presence of testosterone. We have demonstrated that maintenance of trkB receptors with testosterone may be necessary to permit the trophic effects of BDNF in supporting dendritic morphology after axotomy. Together, these findings suggest that testosterone regulates neuroprotective effects on spinal motoneurons through a variety of mechanisms, and support a role for testosterone as a neurotherapeutic agent in the injured nervous system.